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1.  Parental smoking and spirometric indices in children 
Thorax  1998;53(10):884-893.
BACKGROUND—A systematic quantitative review was conducted of the evidence relating parental smoking to spirometric indices in children.
METHODS—An electronic search of the Embase and Medline databases was completed in April 1997 and identified 692 articles from which we included four studies in neonates, 42 cross-sectional studies in school aged children (22 were included in a meta-analysis), and six longitudinal studies of lung function development.
RESULTS—In a pooled analyses of 21 surveys of school aged children the percentage reduction in forced expiratory volume in one second (FEV1) in children exposed to parental smoking compared with those not exposed was 1.4% (95% CI 1.0 to 1.9). Effects were greater on mid expiratory flow rates (5.0% reduction, 95% CI 3.3 to 6.6) and end expiratory flow rates (4.3% reduction, 95% CI 3.1 to 5.5). Adjustment for potential confounding variables had little effect on the estimates. A number of studies reported clear evidence of exposure response. Where exposure was explicitly identified it was usually maternal smoking. Two studies in neonates have reported effects of prenatal exposure to maternal smoking. Of five cross sectional studies that compared effects of perinatal exposure (retrospectively assessed) with current exposure to maternal smoking in later childhood, the three largest concluded that the major effect was in utero or neonatal exposure. Longitudinal studies suggest a small effect of current exposure on growth in lung function, but with some heterogeneity between studies.
CONCLUSIONS—Maternal smoking is associated with small but statistically significant deficits in FEV1 and other spirometric indices in school aged children. This is almost certainly a causal relationship. Much of the effect may be due to maternal smoking during pregnancy.


PMCID: PMC1745082  PMID: 10193379
2.  Airway hyperresponsiveness, prevalence of chronic respiratory symptoms, and lung function in workers exposed to irritants. 
The association between occupational exposure to airway irritants and the prevalence of chronic respiratory symptoms and level of lung function, and whether these associations were modified by airway hyperresponsiveness, smoking, and a history of allergy were studied in 668 workers from synthetic fibre plants. Respiratory symptoms were recorded with a self administered Dutch version of the British Medical Research Council questionnaire, with additional questions on allergy. Airway responsiveness was measured by a 30 second tidal breathing histamine challenge test. On the basis of job titles and working department, the current state of exposure of all workers was characterised as (1) no exposure, reference group; (2) white collar workers; (3) SO2 HCl, SO4(2); (4) polyester vapour; (5) oil mist and vapour; (6) polyamide and polyester vapour; (7) multiple exposure. Workers exposed to airway irritants were not simultaneously exposed to airborne dust. Airway hyperresponsiveness (AHR), defined as a 20% fall in forced expiratory volume in one second (FEV1) at < or = 32 mg/ml histamine, was present in 23% of the subjects. The association between exposure groups and prevalence of symptoms was estimated by means of multiple logistic regression; the association with level of lung function (forced vital capacity (FVC), FEV1, maximum mid-expiratory flow rate (MMEF)) was estimated by means of multiple linear regression. Both methods allow simultaneous adjustment for potential confounding factors. The exposure groups were associated with a higher prevalence of chronic respiratory symptoms. Lower prevalence of symptoms was found for workers exposed to SO2, HCl, and SO4(2-), most likely due to pre-employment selection procedures. Current smoking, AHR, and a history of allergy were significantly associated with a higher prevalence of chronic respiratory symptoms, independent of each other, and independent of irritant exposure. The association between exposure and prevalence of symptoms was greater in smokers than in ex-smokers and non-smokers. This difference was most clearly seen in the polyester vapour and polyamide and polyester vapour group. No modification of the association between exposure groups and prevalence of symptoms by airway hyperresponsiveness could be shown. The exposure groups were not significantly associated with a lower level of lung function. Adjustment for chronic respiratory symptoms did not change the results. There were no indications of a possible interaction between exposure and AHR, current smoking, or a history of allergy on lung function. Workers of the polyester vapour and the oil mist and vapour group with >10 years of exposure had a lower FEV1 (beta = -295 and -358 ml) and significantly lower MMEF (beta = -1080 and -1247 ml/s; p < 0.05) than the reference group. The number of workers of both group were, however, small (n = 10 and n = 13 respectively). More investigations between low level exposure to irritant and respiratory health.
PMCID: PMC1127893  PMID: 8124460
3.  Relation of passive smoking as assessed by salivary cotinine concentration and questionnaire to spirometric indices in children. 
Thorax  1993;48(1):14-20.
BACKGROUND: Previous studies of the effects of passive exposure to smoke on spirometric indices in children have largely relied on questionnaire measures of exposure. This may have resulted in underestimation of the true effect of passive smoking. Biochemical measures offer the opportunity to estimate recent exposure directly. METHODS: The relation between spirometric indices and passive exposure to tobacco smoke was examined in a large population sample of 5-7 year old children from 10 towns in England and Wales. The effects of passive exposure to smoke on lung function were assessed by means of both salivary cotinine concentration and questionnaire measurements of exposure. Analyses of the relation between spirometric values and cotinine concentrations were based on 2511 children and of the relation between spirometric values and questionnaire measures on 2000 children. RESULTS: Cotinine concentration was negatively associated with all spirometric indices after adjustment for confounding variables, which included age, sex, body size, and social class. The strongest association was with mid expiratory flow rate (FEF50), the fall between the bottom and top fifths of the cotinine distribution being 6%, equivalent to a reduction of 14.3 (95% confidence limits (CL) 8.6, 20.0) ml/s per ng/ml cotinine. Salivary cotinine concentrations were strongly related to exposure to cigarette smoke at home but 88% of children who were from non-smoking households and not looked after by a smoker had detectable cotinine concentrations, 5% being in the top two fifths of the cotinine distribution. A composite questionnaire score based on the number of regular sources of exposure was as strongly related to mid and end expiratory flow rates as the single cotinine measure. The fall in FEF50 per smoker to whom the child was exposed was 51.0 (26.5, 75.5) ml/s. The relationships between the questionnaire score and forced vital capacity (FVC) or forced expiratory volume in one second (FEV1) were not statistically significant. CONCLUSIONS: These effects of passive smoking on respiratory function are consistent with the results of previous studies and, although small in absolute magnitude, may be important if the effects of exposure are cumulative. In children aged 5-7 years the use of a single salivary cotinine concentration as a marker of passive exposure to smoke resulted in clear relationships between exposure and FVC and FEV1, whereas the associations were much weaker and not significant when based on the questionnaire score. The associations between exposure and mid or end expiratory flow rates were of similar magnitude for cotinine concentration and the questionnaire score. The use of salivary cotinine concentration in longitudinal studies may help to determine the extent to which these effects are cumulative or reversible.
PMCID: PMC464228  PMID: 8434347
4.  Lung function, respiratory illness, and passive smoking in British primary school children. 
Thorax  1993;48(1):21-25.
BACKGROUND: Many studies have reported a significant association between parents' smoking and reduced lung function in their children, but often the association has been found to be significant only in relation to maternal smoking. There have been few epidemiological studies on this topic in Britain. METHODS: Spirometry, in 2756 children aged 6.50-11.99 years, was carried out in a representative sample of English children, an inner city and ethnic minority sample, and a Scottish sample. Forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and forced expiratory flow rates of 25-75% and 75-85% (FEF25-75 and FEF75-85) were measured and standardised scores obtained separately for the English representative sample, the Scottish sample and subgroups in the inner city sample, white and Afro-Caribbean children and those originating from the Indian subcontinent. Multiple regression analyses were used to assess associations of FVC, FEV1, FEF25-75 and FEF75-85 with the passive smoking and respiratory illness, with adjustment for a large number of potential confounders. Passive smoking was defined in terms of reported number of cigarettes smoked at home by each parent. The respiratory symptoms and illnesses assessed were wheeze, asthma and bronchitis attacks, cough in the morning, and cough at any other time as reported by parents. RESULTS: Maternal smoking, but not paternal smoking, was associated with reduced FEF25-75 and FEF75-85 in boys. No association was found between passive smoking and lung function in girls, but in an analysis including both sexes the interaction of sex and parental smoking on lung function was not significant. With few exceptions, FEV1, FEF25-75 and FEF75-85 were reduced in children with wheeze and asthma attacks. CONCLUSIONS: The effect of passive smoking may depend on the close contact of a parent with a susceptible child as only maternal smoking in boys was significantly associated with impaired lung function. However, this explanation remains unsubstantiated. A parent's report of wheeze and asthma attacks in the child is reflected in reduced lung function.
PMCID: PMC464230  PMID: 8434348
5.  Household environmental tobacco smoke and risks of asthma, wheeze and bronchitic symptoms among children in Taiwan 
Respiratory Research  2010;11(1):11.
Background
Although studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent.
Methods
We conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms.
Results
The lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87).
Conclusion
We concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.
doi:10.1186/1465-9921-11-11
PMCID: PMC2828425  PMID: 20113468
6.  Variation in the GST mu Locus and Tobacco Smoke Exposure as Determinants of Childhood Lung Function 
Rationale: The glutathione S-transferases (GSTs) are important detoxification enzymes.
Objectives: To investigate effects of variants in GST mu genes on lung function and assess their interactions with tobacco smoke exposure.
Methods: In this prospective study, 14,836 lung function measurements were collected from 2,108 children who participated in two Southern California cohorts. For each child, tagging single nucleotide polymorphisms in GSTM2, GSTM3, GSTM4, and GSTM5 loci were genotyped. Using principal components and haplotype analyses, the significance of each locus in relation to level and growth of FEV1, maximum midexpiratory flow rate (MMEF), and FVC was evaluated. Interactions between loci and tobacco smoke on lung function were also investigated.
Measurements and Main Results: Variation in the GST mu family locus was associated with lower FEV1 (P = 0.01) and MMEF (0.04). Two haplotypes of GSTM2 were associated with FEV1 and MMEF, with effect estimates in opposite directions. One haplotype in GSTM3 showed a decrease in growth for MMEF (−164.9 ml/s) compared with individuals with other haplotypes. One haplotype in GSTM4 showed significantly decreased growth in FEV1 (−51.3 ml), MMEF (−69.1 ml/s), and FVC (−44.4 ml), compared with all other haplotypes. These results were consistent across two independent cohorts. Variation in GSTM2 was particularly important for FVC and FEV1 among children whose mothers smoked during pregnancy.
Conclusions: Genetic variation across the GST mu locus is associated with 8-year lung function growth. Children of mothers who smoked during pregnancy and had variation in GSTM2 had lower lung function growth.
doi:10.1164/rccm.200809-1384OC
PMCID: PMC2720124  PMID: 19151192
FEV1; in utero; glutathione S-transferase; tobacco smoke
7.  Respiratory health of workers exposed to metal dusts and foundry fumes in a copper refinery. 
OBJECTIVES--To assess airflow limitation in workers exposed long term to metal dust, the prevalence of pleural plaques in those workers exposed in the past to asbestos, the influence of pleural plaques on lung function, and the possible association with airway disease caused by asbestos. METHODS--A cross sectional and longitudinal (seven year) survey of 494 long term (mean (SEM) 21(1) years) workers in a copper refinery was carried out from medical questionnaires, chest radiographs, and forced spirometry. RESULTS--The prevalence of lifetime non-smokers was 19%, current smokers 39%, and ex-smokers 42%. The prevalence of chronic obstructive pulmonary diseases (COPD) (forced expiratory volume in one second (FEV1) < 80% predicted) was 5%, small airway dysfunction (SAD) (maximal mid-expiratory flow (MMEF) < 60% predicted) was 7%, and this did not differ from the control population. The COPD and SAD were associated with cumulative smoking index but not with the cumulative work years at the plant or with any type of work at the plant. The mean (SEM) reduction of FEV1 was 20(7) ml in non-smokers, 26(4) ml in smokers, and 26(5) ml in ex-smokers (P > 0.05). In the smokers and ex-smokers with COPD, the loss of FEV1 was 53(10) (P < 0.02). The prevalence of pleural plaques was 11% (P < 0.0001); pleural plaques were found in older workers with known exposure to asbestos. The pleural plaques were circumscribed and associated with a non-significant 196 ml reduction in forced vital capacity (FVC) and non-significant reduction of FVC over time. The pleural plaques were not associated with COPD or SAD. The cumulative smoking index obtained by a technician did not differ from that by a chest physician. CONCLUSIONS--Despite exposures to asbestos that produced pleural plaques and exposures to metal dusts and foundry fumes the long term workers of this plant did not have excessive prevalence of COPD or SAD. The data suggest that low level long term exposure to metal dusts, gases, and foundry fumes do not necessarily cause respiratory dysfunction, circumscribed pleural plaques with low grades of width and extent do not reduce FVC significantly, and exposure to asbestos dust that produced pleural plaques does not necessarily produce airway dysfunction.
PMCID: PMC1128188  PMID: 7735395
8.  Lung function at one month of age as a risk factor for infant respiratory symptoms in a high risk population 
Thorax  2002;57(5):388-392.
Background: Abnormal premorbid lung function is a risk factor for subsequent wheezing in children with one or no atopic parent. This study was undertaken to establish whether early lung function in high risk infants (both parents atopic) was a risk factor for respiratory symptoms in infancy and to examine the influence of maternal asthma, smoking, and allergen exposure during pregnancy on any association.
Methods: Infants were recruited from the NAC Manchester Asthma and Allergy Study cohort at birth. Partial forced expiratory flow volume technique under sedation was carried out to determine maximal flow at FRC (V'maxFRC). Children were followed prospectively and parents completed a standard respiratory questionnaire at one year of age.
Results: Sixty nine term infants (34 boys; 88% mothers non-smokers; no household pets) underwent respiratory function testing. Size adjusted V'maxFRC was significantly lower in infants who had recurrent wheeze during the first year of life (mean 1.3 ml/s/cm, 95% CI 0.99 to 1.60) than in those who did not (mean 2.03 ml/s/cm, 95% CI 1.71 to 2.36; p=0.01). V'maxFRC was also significantly lower in infants who had recurrent cough symptoms. In multivariate regression analysis, when adjusted for age at test, sex, maternal asthma, smoking and maternal mattress Der 1 levels, a lower size adjusted V'maxFRC score remained strongly associated with wheezing (OR 0.37, 95% CI 0.18 to 0.77, p=0.007). Maternal smoking also remained an independent risk factor (OR 29.85, 95% CI 2.46 to 362.5, p=0.008).
Conclusion: Significantly diminished lung function was present in high risk infants who subsequently wheezed and coughed. This was independent of maternal exposure to mite allergen, asthma, and smoking during pregnancy.
doi:10.1136/thorax.57.5.388
PMCID: PMC1746314  PMID: 11978912
9.  Synergistic Impaired Effect between Smoking and Manganese Dust Exposure on Pulmonary Ventilation Function in Guangxi Manganese-Exposed Workers Healthy Cohort (GXMEWHC) 
PLoS ONE  2015;10(2):e0116558.
Purpose
The aims of this study were to investigate the effects of manganese (Mn) dust exposure on lung functions and evaluate the potential synergistic effect between smoking and Mn dust exposure among refinery workers.
Methods
A retrospective study including 1658 workers in a ferromanganese refinery was conducted, with subjects who were from the Guangxi manganese-exposed workers healthy cohort (GXMEWHC). Based on the Mn manganese cumulative exposure index (Mn-CEI), all subjects were divided into the low exposure group (n = 682) and the high exposure group (n = 976). A pulmonary function test was performed using an electronic spirometer, including the values and percentages of FVC, FEV1, FEV1/FVC, MMEF, PEFR, MVV, respectively.
Results
No significant effect of Mn dust exposure on the pulmonary function was found in the female workers (all p>0.05). However, there was an obvious decrease in the male workers in the high exposure group compared with those in the low exposure group (FVC -60 ml, FEV1 -120 ml, MMEF -260 ml/s, MVV -5.06 L, all p<0.05). In the high exposure group, the reduction in FVC% predicted, MMEF and MMEF% predicted was 1.0%, 210 mL/s, and 4.9%, respectively. In particular, among the exposed subjects smokers had a statistically significant decrease in lung function compared with non-smokers and the reduction in FVC% predicted, MMEF and MMEF% predicted was 1.0%, 210 mL/s, and 4.9%, respectively (p<0.05). Partial correlation analysis showed that there was also negative correlation between Mn-CEI and decreased changes in MMEF (r = -0.159, p = 0.018) and also MMEF% predicted (r = -0.163, p = 0.015).
Conclusions
Mn dust can impair the pulmonary ventilation function of male workers but not females, and individual smoking habits and manganese exposure had a synergistic effect on the lung function decrease.
doi:10.1371/journal.pone.0116558
PMCID: PMC4321994  PMID: 25664879
10.  Exposure to Tobacco Smoke in Utero and Subsequent Plasma Lipids, ApoB, and CRP among Adult Women in the MoBa Cohort 
Environmental Health Perspectives  2012;120(11):1532-1537.
Background: Recent findings suggest that maternal smoking during pregnancy may play a role in the development of metabolic alterations in offspring during childhood. However, whether such exposure increases the risk of developing similar metabolic alterations during adulthood is uncertain.
Objective: We evaluated the association of in utero exposure to maternal tobacco smoke with plasma lipids, apolipoprotein B (apoB), and C-reactive protein (CRP) in adulthood.
Methods: The study was based on a subsample of the Norwegian Mother and Child Cohort Study (MoBa) and included 479 pregnant women with plasma lipids, apoB, and CRP measurements. Information on in utero exposure to tobacco smoke, personal smoking, and other factors were obtained from the women by a self-completed questionnaire at enrollment, at approximately 17 weeks of gestation.
Results: Women exposed to tobacco smoke in utero had higher triglycerides [10.7% higher; 95% confidence interval (CI): 3.9, 17.9] and lower high-density lipoprotein cholesterol (HDL) (–1.9 mg/dL; 95% CI: –4.3, 0.5) compared with unexposed women, after adjusting for age, physical activity, education, personal smoking, and current body mass index (BMI). Exposed women were also more likely to have triglycerides ≥ 200 mg/dL [adjusted odds ratio (aOR) = 2.5; 95% CI: 1.3, 5.1] and HDL < 50 mg/dL (aOR = 2.3; 95% CI: 1.1, 5.0). Low-density lipoprotein cholesterol, total cholesterol, and apoB were not associated with the exposure. CRP was increased among exposed women; however, after adjustment for BMI, the association was completely attenuated.
Conclusions: In this population, in utero exposure to tobacco smoke was associated with high triglycerides and low HDL in adulthood, 18–44 years after exposure.
doi:10.1289/ehp.1104563
PMCID: PMC3556606  PMID: 22814200
clinical chemistry; C-reactive protein; metabolic syndrome; plasma lipids; prenatal exposure delayed effects; smoking; women
11.  Pulmonary effects of passive smoking: the Indian experience 
Tobacco Induced Diseases  2002;1(2):129-136.
There are only a few studies done on pulmonary effects of passive smoking from India, which are summarized in this paper. Several vernacular tobacco products are used in India, bidis (beedis) being the commonest form of these. Bidis contain a higher concentration of nicotine and other tobacco alkaloids compared to the standard cigarettes (e.g., the sum of total nicotine and minor tobacco alkaloids was 37.5 mg in bidi compared to 14–16 mg in Indian or American cigarettes in one study). A large study performed on 9090 adolescent school children demonstrated environmental tobacco smoke (ETS) exposure to be associated with an increased risk of asthma. The odds ratio for being asthmatic in ETS-exposed as compared to ETS-unexposed children was 1.78 (95% CI: 1.33–2.31). Nearly one third of the children in this study reported non-specific respiratory symptoms and the ETS exposure was found to be positively associated with the prevalence of each symptom. Passive smoking was also shown to increase morbidity and to worsen the control of asthma among adults. Another study demonstrated exposure to ETS was a significant trigger for acute exacerbation of asthma. Increased bronchial hyper-responsiveness was also demonstrated among the healthy nonsmoking adult women exposed to ETS. Passive smoking leads to subtle changes in airflow mechanics. In a study among 50 healthy nonsmoking women passively exposed to tobacco smoke and matched for age with 50 unexposed women, forced expiratory volume in first second (FEV1) and peak expiratory flow (PEF) were marginally lower among the passive smokers (mean difference 0.13 L and 0.20 L-1, respectively), but maximal mid expiratory flow (FEF25–75%), airway resistance (Raw) and specific conductance (sGaw) were significantly impaired. An association between passive smoking and lung cancer has also been described. In a study conducted in association with the International Agency for Research on Cancer, the exposure to ETS during childhood was strongly associated with an enhanced incidence of lung cancer (OR = 3.9, 95% CI 1.9–8.2). In conclusions several adverse pulmonary effects of passive smoking, similar to those described from the western and developed countries, have been described from India.
doi:10.1186/1617-9625-1-2-129
PMCID: PMC2671649  PMID: 19570253
12.  Pulmonary effects of passive smoking: the Indian experience 
Tobacco Induced Diseases  2002;1(1):10.
There are only a few studies done on pulmonary effects of passive smoking from India, which are summarized in this paper. Several vernacular tobacco products are used in India, bidis (beedis) being the commonest form of these. Bidis contain a higher concentration of nicotine and other tobacco alkaloids compared to the standard cigarettes (e.g., the sum of total nicotine and minor tobacco alkaloids was 37.5 mg in bidi compared to 14–16 mg in Indian or American cigarettes in one study). A large study performed on 9090 adolescent school children demonstrated environmental tobacco smoke (ETS) exposure to be associated with an increased risk of asthma. The odds ratio for being asthmatic in ETS-exposed as compared to ETS-unexposed children was 1.78 (95% CI: 1.33–2.31). Nearly one third of the children in this study reported non-specific respiratory symptoms and the ETS exposure was found to be positively associated with the prevalence of each symptom. Passive smoking was also shown to increase morbidity and to worsen the control of asthma among adults. Another study demonstrated exposure to ETS was a significant trigger for acute exacerbation of asthma. Increased bronchial hyper-responsiveness was also demonstrated among the healthy nonsmoking adult women exposed to ETS. Passive smoking leads to subtle changes in airflow mechanics. In a study among 50 healthy nonsmoking women passively exposed to tobacco smoke and matched for age with 50 unexposed women, forced expiratory volume in first second (FEV1) and peak expiratory flow (PEF) were marginally lower among the passive smokers (mean difference 0.13 L and 0.20 L-1, respectively), but maximal mid expiratory flow (FEF25–75%), airway resistance (Raw) and specific conductance (sGaw) were significantly impaired. An association between passive smoking and lung cancer has also been described. In a study conducted in association with the International Agency for Research on Cancer, the exposure to ETS during childhood was strongly associated with an enhanced incidence of lung cancer (OR = 3.9, 95% CI 1.9–8.2). In conclusions several adverse pulmonary effects of passive smoking, similar to those described from the western and developed countries, have been described from India.
doi:10.1186/1617-9625-1-10
PMCID: PMC2669550
13.  Familial aggregation of FEF25–75 and FEF25–75/FVC in families with severe, early onset COPD 
Thorax  2004;59(5):396-400.
Background: The Boston Early-Onset COPD study showed that current or ex-smoking first degree relatives of severe early onset COPD probands have significantly lower forced expiratory volume in 1 second (FEV1) and FEV1/forced vital capacity (FVC) values than current or ex-smoking control subjects, which suggests the existence of genetic risk factors for the development of COPD in response to cigarette smoking. We hypothesised that first degree relatives of early onset COPD probands may also have lower values of spirometric parameters such as forced expiratory flow at the mid-portion of forced vital capacity (FEF25–75) and FEF25–75/FVC.
Methods: Using generalised estimating equations, FEF25–75 and FEF25–75/FVC were analysed in 333 first degree relatives of probands with severe early onset COPD and 83 population based controls; analyses were also performed on data stratified by smoking status. Narrow sense heritability estimates were calculated using a variance component approach.
Results: Significantly lower FEF25–75 and FEF25–75/FVC were observed in smoking (FEF25–75: ß –0.788 l/s (95% CI –1.118 to –0.457), FEF25–75/FVC: ß –20.4% (95% CI –29.3 to –11.6, p<0.0001 for both phenotypes) and non-smoking (FEF25–75: ß –0.357 l/s (95% CI –0.673 to –0.041, p = 0.0271), FEF25–75/FVC: ß –9.5% (95% CI –17.1 to –1.9, p = 0.0145)) first degree relatives of early onset COPD probands. Narrow sense heritability estimates for FEF25–75 (h2 = 0.38) and FEF25–75/FVC (h2 = 0.45) were similar to those for FEV1 and FEV1/FVC.
Conclusion: Lower values of FEF25–75 and FEF25–75/FVC in non-smoking first degree relatives of early onset COPD probands than in controls suggest a genetic susceptibility to develop obstructive lung disease, independent of smoking, which is magnified by exposure to deleterious environments as suggested by the further decrements in FEF25–75 and FEF25–75/FVC seen in smoking first degree relatives. FEF25–75 and FEF25–75/FVC have high heritability and are important intermediate phenotypes for inclusion in genetic epidemiological studies of COPD.
doi:10.1136/thx.2003.012856
PMCID: PMC1747013  PMID: 15115866
14.  Parental smoking during pregnancy and risk of overweight and obesity in the daughter 
Objective
Emerging evidence suggests that prenatal exposures may affect long-term health outcomes. In utero exposure to smoking is associated with an increased risk of overweight and obesity in children and adolescents. However, few studies have examined how prenatal exposure to parental smoking influences risk of obesity in adulthood and whether these associations are independent of childhood and adolescent adiposity. The aim of the current study was to investigate whether prenatal exposure to parental smoking influences body size in adulthood and whether any association may be mediated by childhood and adolescent body size.
Methods
We investigated the association between parental smoking during pregnancy and risk of overweight and obesity in adulthood and at age 18, and adiposity during childhood among 35,370 participants in the Nurses’ Health Study II. Data on smoking during pregnancy and socioeconomic variables were provided by the mothers, and anthropometric data and adult risk factors were reported by participants.
Results
After adjustment for socioeconomic and behavioral variables, maternal smoking during pregnancy was associated with adiposity at ages 5–10, age 18, and during adulthood. For age 18 overweight the ORs (95% CIs) for 1–14, 15–24, and 25+cigarettes/day were 1.13 (1.18–1.50), 1.40 (1.20–1.64), and 1.15 (0.79–1.69) and for obesity were 1.41 (1.14–1.75), 1.69 (1.31–2.18), and 2.36 (1.44–3.86). The corresponding ORs (95% CIs) for obesity in adulthood were 1.26 (1.16–1.37), 1.46 (1.30–1.63), and 1.43 (1.10–1.86). Risk of adiposity was not increased among daughters whose mothers stopped smoking during the first trimester (OR [95% CI] for overweight (1.03 [95% CI 0.90–1.17] and obesity (1.12 [95% CI 0.97–1.30]). Women whose fathers smoked during pregnancy were also at increased risk of overweight and obesity in adulthood with covariate-adjusted ORs (95% CIs) for obesity of 1.19 (1.11–1.29) for 1–14 cigarettes/day, 1.27 (1.18–1.37) for 15–24 cigarettes/day, and 1.40 (1.27–1.54) for 25+ cigarettes/day compared to fathers who did not smoke (ptrend<0.0001). Paternal smoking during pregnancy was also associated with an increased risk of obesity at age 18 among those whose fathers smoked 15 or more cigarettes/day but was not associated with childhood body size.
Conclusions
Maternal smoking during pregnancy was associated in a dose-response manner with overweight and obesity in the daughter through adolescence and adult life. Smoking cessation during the first trimester appears to mitigate this excess risk.
Paternal smoking was also associated with risk of overweight and obesity of the adult daughter and this association persisted after adjustment for maternal smoking.
doi:10.1038/ijo.2013.101
PMCID: PMC3795801  PMID: 23736356
pregnancy; prenatal programming; cigarette smoking; obesity
15.  Ethnic Variability in Persistent Asthma After In Utero Tobacco Exposure 
Pediatrics  2011;128(3):e623-e630.
BACKGROUND:
The effects of in utero tobacco smoke exposure on childhood respiratory health have been investigated, and outcomes have been inconsistent.
OBJECTIVE:
To determine if in utero tobacco smoke exposure is associated with childhood persistent asthma in Mexican, Puerto Rican, and black children.
PATIENTS AND METHODS:
There were 295 Mexican, Puerto Rican, and black asthmatic children, aged 8 to 16 years, who underwent spirometry, and clinical data were collected from the parents during a standardized interview. The effect of in utero tobacco smoke exposure on the development of persistent asthma and related clinical outcomes was evaluated by logistic regression.
RESULTS:
Children with persistent asthma had a higher odds of exposure to in utero tobacco smoke, but not current tobacco smoke, than did children with intermittent asthma (odds ratio [OR]: 3.57; P = .029). Tobacco smoke exposure from parents in the first 2 years of life did not alter this association. Furthermore, there were higher odds of in utero tobacco smoke exposure in children experiencing nocturnal symptoms (OR: 2.77; P = .048), daily asthma symptoms (OR: 2.73; P = .046), and emergency department visits (OR: 3.85; P = .015) within the year.
CONCLUSIONS:
Exposure to tobacco smoke in utero was significantly associated with persistent asthma among Mexican, Puerto Rican, and black children compared with those with intermittent asthma. These results suggest that smoking cessation during pregnancy may lead to a decrease in the incidence of persistent asthma in these populations.
doi:10.1542/peds.2011-0640
PMCID: PMC3164096  PMID: 21859918
asthma; tobacco; Latino; African American; pregnancy
16.  Effect of GSTM2-5 polymorphisms in relation to tobacco smoke exposures on lung function growth: a birth cohort study 
Background
Genetic variation within GSTM2-5 genes may interfere with detoxification of environmental compounds, thereby having a detrimental effect on lung function following exposures such as tobacco smoke. We aim to investigate the influence of variants and associated methylation in the GSTM gene cluster with changes in lung function growth during adolescence.
Methods
Growth in forced expiratory volume (FEV1), forced vital capacity (FVC), and change in FEV1/FVC ratio measures were obtained from children in the Isle of Wight birth cohort at ages 10 and 18. Illumina GoldenGate assays were used to genotype 10 tagging polymorphisms from GSTM2 (rs574344 and rs12024479), GSTM3 (rs1537236, rs7483, and rs10735234), GSTM4 (rs668413, rs560018, and rs506008), and GSTM5 (rs929166 and rs11807) genes. Diplotypes were generated in the software Phase 3.0.2. DNA methylation was measured in over 450,000 CpG sites using the Infinium HumanMethylation450 BeadChip (Illumina 450K) in a subsample of 245 18-year olds from the Isle of Wight birth cohort. Gender, age, in utero smoke exposure, secondhand smoke exposure (SHS), and current smoking status were assessed via questionnaire; smoke exposures were validated with urine cotinine. We used linear mixed models to estimate the effect of GSTM diplotypes on lung function across time and examine interactions with tobacco smoke.
Results
1,121 (77%) out of 1,456 children had information on lung function at ages 10 or 18. After adjustment for false discovery rate, one diplotype in GSTM3 had a detrimental effect on changes in FEV1 (p=0.03), and another diplotype in GSTM3 reduced FVC (p=0.02) over time. No significant interactions with smoking were identified. SHS significantly modified the relationship between diplotypes and methylation levels in one GSTM2 CpG site; however, this site did not predict lung function outcomes at age 18. Joint effects of GSTM loci and CpG sites located within these loci on adolescent lung growth were detected.
Conclusions
Diplotypes within GSTM2-5 genes are associated with lung function growth across adolescence, but do not appear to modify the effect of tobacco smoke exposures on adolescent lung growth. Interactions between DNA methylation and diplotypes should be taken into account to gain further understanding on lung function in adolescence.
doi:10.1186/1471-2466-13-56
PMCID: PMC3846453  PMID: 24004509
Smoking; Lung function; Diplotype; Human; Longitudinal study; Epigenetics; Methylation quantitative trait loci
17.  Effects of In Utero and Childhood Tobacco Smoke Exposure and β2-Adrenergic Receptor Genotype on Childhood Asthma and Wheezing 
Pediatrics  2008;122(1):e107-e114.
Objective
Associations between single-nucleotide polymorphisms in the β2-adrenergic receptor gene and asthma and wheeze have been inconsistent. Recent studies indicated that tobacco smoke affects β2-adrenergic receptor gene expression and associations of β2-adrenergic receptor gene variants with asthma in adults. We aimed to investigate the joint effects of in utero and childhood secondhand tobacco smoke exposure and 2 well-characterized functional single-nucleotide polymorphisms (Arg16Gly and Glu27Gln) of β2-adrenergic receptor gene on asthma and wheezing in 3128 non-Hispanic and Hispanic white children of the Children's Health Study.
Methods
We fitted logistic regression models to estimate odds ratios and 95% confidence intervals for the independent and joint effects of these single-nucleotide polymorphisms and in utero and secondhand tobacco smoke exposure on asthma and wheeze outcomes.
Results
Exposures to in utero maternal smoking and secondhand tobacco smoke were associated with wheezing. Children who were homozygous for the Arg16 allele and were exposed to maternal smoking in utero were at a threefold increased risk for lifetime wheeze compared with children who were unexposed and had at least 1 Gly16 allele. We found similar joint effects of secondhand tobacco smoke and Arg16Gly with wheezing. The risk for lifetime, current, and nocturnal wheeze increased with the number of smokers at home among Arg16 homozygous children. The results were consistent in 2 cohorts of children recruited in 1993 and 1996. Diplotype-based analyses were consistent with the single-nucleotide polymorphism–specific results. No associations were found for Glu27Gln.
Conclusions
Both in utero and childhood exposure to tobacco smoke were associated with an increased risk for wheeze in children, and the risks were greater for children with the Arg16Arg genotype or 2 copies of the Arg16–Gln27 diplotype. Exposures to smoking need to be taken into account when evaluating the effects of β2-adrenergic receptor gene variants on respiratory health outcomes.
doi:10.1542/peds.2007-3370
PMCID: PMC2748980  PMID: 18558635
β-2 adrenergic receptor; prenatal exposure; secondhand-smoke exposure; asthma; wheeze
18.  Parental smoking in childhood and adult obstructive lung disease: results from the European Community Respiratory Health Survey 
Thorax  2004;59(4):295-302.
Background: Early exposure to parental smoking appears to influence the development of the airways and predispose to respiratory symptoms. A study was undertaken to determine whether the consequences of parental smoking could be traced in adulthood.
Methods: Information from interviewer-led questionnaires was available for 18 922 subjects aged 20–44 years from random population samples in 37 areas participating in the European Community Respiratory Health Survey. Lung function data were available for 15 901 subjects.
Results: In men, father's smoking in childhood was associated with more respiratory symptoms (ORwheeze 1.13 (95% CI 1.00 to 1.28); never smokers: ORwheeze 1.21 (95% CI 0.96 to 1.50)) and there was a dose-dependent association between number of parents smoking and wheeze (one: OR 1.08 (95% CI 0.94 to 1.24); both: OR 1.24 (95% CI 1.05 to 1.47); ptrend = 0.010). A reduced ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) was related to father's smoking (-0.3% (95% CI -0.6 to 0)) and number of parents smoking (ptrend <0.001) among men. In women, mother's smoking was associated with more respiratory symptoms and poorer lung function (ORwheeze 1.15 (95% CI 1.01 to 1.31), never smokers: ORwheeze 1.21 (95% CI 0.98–1.51); FEV1 -24 ml (95% CI -45 to -3); FEV1/FVC ratio -0.6% (95% CI -0.9 to -0.3)). These effects were possibly accounted for by maternal smoking in pregnancy (ORwheeze 1.39 (95% CI 1.17 to 1.65); FEV1 -23 ml (95% CI -52 to 7); FEV1/FVC ratio -0.9% (95% CI -1.3 to -0.4)) as there was no association with paternal smoking among women (interaction by sex, p<0.05). These results were homogeneous across centres.
Conclusion: Both intrauterine and environmental exposure to parental tobacco smoking was related to more respiratory symptoms and poorer lung function in adulthood in this multicultural study. The age window of particular vulnerability appeared to differ by sex, postnatal exposure being important only in men and a role for prenatal exposure being more evident in women.
doi:10.1136/thx.2003.009746
PMCID: PMC1763798  PMID: 15047948
19.  GST-omega genes interact with environmental tobacco smoke on adult level of lung function 
Respiratory Research  2013;14(1):83.
Background
Lung growth in utero and lung function loss during adulthood can be affected by exposure to environmental tobacco smoke (ETS). The underlying mechanisms have not been fully elucidated. Both ETS exposure and single nucleotide polymorphisms (SNPs) in Glutathione S-Transferase (GST) Omega genes have been associated with the level of lung function. This study aimed to assess if GSTO SNPs interact with ETS exposure in utero and during adulthood on the level of lung function during adulthood.
Methods
We used cross-sectional data of 8,128 genotyped participants from the LifeLines cohort study. Linear regression models (adjusted for age, sex, height, weight, current smoking, ex-smoking and packyears smoked) were used to analyze the associations between in utero, daily and workplace ETS exposure, GSTO SNPs, the interaction between ETS and GSTOs, and level of lung function (FEV1, FEV1/FVC). Since the interactions between ETS and GSTOs may be modified by active tobacco smoking we additionally assessed associations in never and ever smokers separately. A second sample of 5,308 genotyped LifeLines participants was used to verify our initial findings.
Results
Daily and workplace ETS exposure was associated with significantly lower FEV1 levels. GSTO SNPs (recessive model) interacted with in utero ETS and were associated with higher levels of FEV1, whereas the interactions with daily and workplace ETS exposure were associated with lower levels of FEV1, effects being more pronounced in never smokers. The interaction of GSTO2 SNP rs156697 with in utero ETS associated with a higher level of FEV1 was significantly replicated in the second sample. Overall, the directions of the interactions of in utero and workplace ETS exposure with the SNPs found in the second (verification) sample were in line with the first sample.
Conclusions
GSTO genotypes interact with in utero and adulthood ETS exposure on adult lung function level, but in opposite directions.
doi:10.1186/1465-9921-14-83
PMCID: PMC3751364  PMID: 23937118
Genes; Environmental tobacco smoke; Lung function
20.  In utero exposure to maternal smoking and women's risk of fetal loss in the Norwegian Mother and Child Cohort (MoBa) 
BACKGROUND
Whether in utero exposure to tobacco smoke increases a woman's risk of fetal loss later in life is unknown, though data on childhood exposure suggest an association may exist. This study evaluated the association between in utero exposure to tobacco smoke and fetal loss in the Norwegian Mother and Child Cohort Study (MoBa), which enrolled ∼40% of the pregnant women in Norway from 1999 to 2008.
METHODS
Information on exposure to tobacco smoke in utero, the woman's own smoking behavior during pregnancy and other factors was obtained by a questionnaire completed at ∼17 weeks of gestation. Subsequent late miscarriage (fetal death <20 weeks) and stillbirth (fetal death ≥20 weeks) were ascertained from the Norwegian Medical Birth Registry. This analysis included 76 357 pregnancies (MoBa data set version 4.301) delivered by the end of 2008; 59 late miscarriages and 270 stillbirths occurred. Cox proportional hazards models were fit for each outcome and for all fetal deaths combined.
RESULTS
The adjusted hazard ratio (HR) of late miscarriage was 1.23 [95% confidence interval (CI), 0.72–2.12] in women with exposure to maternal tobacco smoke in utero when compared with non-exposed women. The corresponding adjusted HR for stillbirths was 1.11 (95% CI, 0.85–1.44) and for all fetal deaths combined, it was 1.12 (95% CI, 0.89–1.43).
CONCLUSIONS
The relatively wide CI around the HR for miscarriage reflected the limited power to detect an association, due to enrollment around 17 weeks of gestation. However, for in utero exposure to tobacco smoke and risk of stillbirth later in life, where the study power was adequate, our data provided little support for an association.
doi:10.1093/humrep/deq334
PMCID: PMC3024897  PMID: 21147823
tobacco smoking; in utero exposure; miscarriage; pregnancy; stillbirth
21.  Association between lung function and cognition among children in a prospective birth cohort study 
Psychosomatic medicine  2008;70(3):356-362.
Objectives
While a growing number of studies have demonstrated a relationship between lung function and cognition among adults, this relationship has not been studied among children. We examined the relationship between lung function and cognition among children in the Maternal-Infant Smoking Study of East Boston, a prospective cohort of women and children enrolled prior to 20 weeks of gestation.
METHODS
At 6 years of age, children completed lung function tests. At 9 years of age, the Wide Range Assessment of Memory and Learning (WRAML) and Kaufman Brief Intelligence Test (K-BIT) were administered. Linear regression was used to assess the relationship between cognition and lung function adjusting for race, maternal education, child's gender, age, height, birthweight, asthma, allergies, lower respiratory infections, blood lead level, in utero and second hand tobacco exposure.
RESULTS
The sample of 165 children included 53% girls and 52% Hispanic. Mean (± SD) forced expiratory volume in one second (FEV1) was 1.26L + 0.2; mean forced vital capacity (FVC) was 1.37L + 0.2. In multivariate regression, a one percent increase from expected FEV1 was associated with increases in the matrices and composite subscales of the KBIT (p < .05), and in the verbal and learning subscales of the WRAML (p <.10). FVC was associated with increases in the composite and matrices subscale of the KBIT and in the visual and learning subscales of the WRAML (all p < .05).
CONCLUSION
Increased lung function was associated with increased cognitive development among children after adjusting for tobacco exposure, birthweight and peak blood lead. Lung and cognitive function may operate under common regulatory processes and thus have shared vulnerabilities to a host of environmental factors during development.
doi:10.1097/PSY.0b013e3181656a5a
PMCID: PMC3086642  PMID: 18378869
cognitive function; lung function; children
22.  Cross shift changes in lung function among bar and restaurant workers before and after implementation of a smoking ban 
Objective
To study possible cross shift effects of environmental tobacco smoke (ETS) on pulmonary function among bar and restaurant employees before and after the implementation of a smoking ban in Norway.
Methods
The study included 93 subjects employed in 13 different establishments in Oslo. They were examined at the beginning and end of a workshift both while ETS exposure was present and when smoking was banned. The mean exposure level of nicotine and total dust before the ban was 28 μg/m3 (range 3–65) and 275 μg/m3 (range 81–506), respectively. Following the smoking ban, the mean level of nicotine and total dust was 0.6 μg/m3 and 77 μg/m3, respectively. Assessment of lung function included dynamic lung volumes and flows.
Results
The cross shift reduction in forced vital capacity (FVC) among 69 subjects participating in both examinations changed from 81 ml (SD 136) during exposure to ETS to 52 ml (SD 156) (p = 0.24) following the smoking ban. The reduction in forced expired volume in one second (FEV1) during a workshift, was borderline significantly reduced when comparing the situation before and after the intervention, by 89 ml (SD = 132) compared to 46 ml (SD = 152) (p = 0.09), respectively. The reduction in forced mid‐expiratory flow rate (FEF25–75%) changed significantly from 199 ml/s (SD = 372) to 64 ml/s (SD = 307) (p = 0.01). Among 26 non‐smokers and 11 asthmatics, the reduction in FEV1 and FEF25–75% was significantly larger during ETS exposure compared to after the smoking ban. There was an association between the dust concentration and decrease in FEF25–75% before the ban among non‐smokers (p = 0.048).
Conclusions
This first study of cross shift changes before and after the implementation of a smoking ban in restaurants and bars shows a larger cross shift decrease in lung function before compared with after the implementation of the ban.
doi:10.1136/oem.2005.024638
PMCID: PMC2092508  PMID: 16551754
environmental tobacco smoke; cross shift; pulmonary function; smoking ban
23.  Maternal smoking during pregnancy increases the risk of recurrent wheezing during the first years of life (BAMSE) 
Respiratory Research  2006;7(1):3.
Background
Exposure to cigarette smoking during foetal and early postnatal life may have implications for lung health. The aim of this study was to assess the possible effects of such exposure in utero on lower respiratory disease in children up to two years of age.
Methods
A birth cohort of 4089 newborn infants was followed for two years using parental questionnaires. When the infant was two months old the parents completed a questionnaire on various lifestyle factors, including maternal smoking during pregnancy and after birth. At one and two years of age information was obtained by questionnaire on symptoms of allergic and respiratory diseases as well as on environmental exposures, particularly exposure to environmental tobacco smoke (ETS). Adjustments were made for potential confounders.
Results
When the mother had smoked during pregnancy but not after that, there was an increased risk of recurrent wheezing up to two years' age, ORadj = 2.2, (95% CI 1.3 – 3.6). The corresponding OR was 1.6, (95% CI 1.2 – 2.3) for reported exposure to ETS with or without maternal smoking in utero. Maternal smoking during pregnancy but no exposure to ETS also increased the risk of doctor's diagnosed asthma up to two years of age, ORadj = 2.1, (95% CI 1.2 – 3.7).
Conclusion
Exposure to maternal cigarette smoking in utero is a risk factor for recurrent wheezing, as well as doctor's diagnosed asthma in children up to two yearsof age.
doi:10.1186/1465-9921-7-3
PMCID: PMC1360665  PMID: 16396689
24.  Relationship between pulmonary function and indoor air pollution from coal combustion among adult residents in an inner-city area of southwest China 
Few studies evaluate the amount of particulate matter less than 2.5 mm in diameter (PM2.5) in relation to a change in lung function among adults in a population. The aim of this study was to assess the association of coal as a domestic energy source to pulmonary function in an adult population in inner-city areas of Zunyi city in China where coal use is common. In a cross-sectional study of 104 households, pulmonary function measurements were assessed and compared in 110 coal users and 121 non-coal users (≥18 years old) who were all nonsmokers. Several sociodemographic factors were assessed by questionnaire, and ventilatory function measurements including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), the FEV1/FVC ratio, and peak expiratory flow rate (PEFR) were compared between the 2 groups. The amount of PM2.5 was also measured in all residences. There was a significant increase in the relative concentration of PM2.5 in the indoor kitchens and living rooms of the coal-exposed group compared to the non-coal-exposed group. In multivariate analysis, current exposure to coal smoke was associated with a 31.7% decrease in FVC, a 42.0% decrease in FEV1, a 7.46% decrease in the FEV1/FVC ratio, and a 23.1% decrease in PEFR in adult residents. The slope of lung function decrease for Chinese adults is approximately a 2-L decrease in FVC, a 3-L decrease in FEV1, and an 8 L/s decrease in PEFR per count per minute of PM2.5 exposure. These results demonstrate the harmful effects of indoor air pollution from coal smoke on the lung function of adult residents and emphasize the need for public health efforts to decrease exposure to coal smoke.
doi:10.1590/1414-431X20144084
PMCID: PMC4230289  PMID: 25296361
Indoor air pollution; Coal combustion; Lung function; Particulate matter
25.  The effect of passive smoking on pulmonary function during childhood 
Postgraduate Medical Journal  1999;75(884):339-341.
Passive smoking, especially of maternal origin, is known to influence adversely the development of children's pulmonary function. In this study, the effect of parental smoking on the pulmonary function of 360 primary school children aged 9-13 (mean 10.8±0.7) years was investigated. Information on parental smoking history was collected using a questionnaire, and spirometric measurements were performed on the children.
All spirometric indices were lower in children who had been passively exposed to parental tobacco smoke than those not exposed. The percentage of households in which at least one parent smoked was 81.5%. This figure was significantly lower for mothers (27.5%) than for fathers (79%). Paternal smoking was associated with reduced levels of forced expiratory flow between 25-75% of vital capacity, peak expiratory flow, and flow rates after 50% and 75% of vital capacity expired (p<0.05). Maternal smoking did not have statistically significant adverse effects on children's pulmonary function. This result might be due to the low occurrence of either pre- or post-natal smoking among mothers and confirms that, in our population, the main target group for anti-tobacco campaigns should be fathers.


Keywords: passive smoking; pulmonary function; tobacco smoke
PMCID: PMC1741251  PMID: 10435167

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