We present a theoretical framework for assessment of exposure to environmental tobacco smoke (ETS), and review current methods in order to provide guidelines for different types of studies. Exposure assessment should include both a quantitative dimension and consideration of time-specificity of exposure. The ultimate aim is to measure the concentrations of ETS encountered by an individual for different time periods in various microenvironments. The first step is to identify an indicator of ETS. Personal monitoring of air nicotine and respirable suspended particulates (RSPs) are the most direct assessment methods. Indirect assessment methods include stationary measurements of tobacco smoke constituents in different microenvironments and/or questionnaire-derived information, modelled with time-activity information. Biomarkers, such as nicotine and/or cotinine in body fluids or hair, can be used as surrogate measures of dose, although they are usually affected by individual processes in the body after exposure. 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 with a long latency period and rare diseases requiring large study populations. Cotinine in body fluids and nicotine concentration in hair can be used to assess cumulative exposure over days or months, respectively. A combination of different methods is often the best approach.
Polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) were analyzed in 167 random human milk samples from urban and rural areas in Finland. Dietary habits and background information on each mother and child were gathered by questionnaire. Body mass indexes (BMI) before pregnancy and delivery in the rural area were 5-10% higher than in the urban area, but fat content of mother's milk was about 10% higher in the urban area. The mean weights of children (+/- standard deviation) were similar in the rural and urban areas among primiparae, 3,500 +/- 597 g and 3,505 +/- 454 g, respectively, although dioxin international toxic equivalents (I-TEQs) were significantly higher in the urban area. The mother's level of education did not affect the weight of the child, but concentrations of PCDDs/PCDFs (I-TEQ, 2,3,4,7,8-Cl5 dibenzofuran,1,2, 3,7,8-Cl5 dibenzodioxin) and PCBs [sum of PCBs (sumPCB), PCB-TEQ, and most PCB congeners] increased with advanced education. This is considered to be due to differences in the mother's consumption of fish. The birth weight, especially of boys, slightly decreased with increasing concentrations of I-TEQ, 2,3,4,7,8-Cl5 dibenzofuran, 1,2,3, 7,8-Cl5 dibenzodioxin, and 2,3,7,8-Cl4 dibenzodioxin; however, when the analysis was restricted to primiparae, there was no statistically significant correlation between birth weight and the concentrations of PCDDs/PCDFs. No correlation was found between the weight of the child and PCBs, PCB-TEQs, or individual PCB congeners in the whole material or among primiparae, or among boys or girls. The concentrations of PCDDs/PCDFs and PCBs inhuman milk were modeled for primiparae by weighing fish consumption, age of mother, milk fat content, and BMI before pregnancy. The linear regression resulted in values of R = 0.67 and 0.30 for the modeled dioxin I-TEQs in the urban and rural areas, respectively, and the corresponding values for sumPCBs of R = 0.60 and 0.11. The increase of PCDD/PCDF body burden was calculated to be on average 0.58 pg I-TEQ/g milk fat/year in the urban area and 0.39 pg I-TEQ/g milk fat/year in the rural area.
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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.
OBJECTIVE: To estimate the effects of the type of day care on respiratory health in preschool children. METHODS: A population-based cross-sectional study of Oslo children born in 1992 was conducted at the end of 1996. A self-administered questionnaire inquired about day care arrangements, children's health, environmental conditions, and family characteristics (n = 3853; response rate, 79%). RESULTS: In logistic regression controlling for confounding, children in day care centers had more often nightly cough (adjusted odds ratio, 1.89; 95% confidence interval, 1.34-2. 67), and blocked or runny nose without common cold (1.55; 1.07-1.61) during the past 12 months compared with children in home care. Poisson regression analysis showed an increased risk of the common cold (incidence rate ratio, 1.21; 1.12-1.30) and otitis media (1.48; 1.22-1.80), and the attributable proportion was 17.4% (95% confidence interval, 10.7-23.1) for the common cold and 32.4% (18. 0-44.4) for otitis media. Early starting age in the day care center increased the risk of developing recurrent otitis media. Also the lifetime risk of doctor-diagnosed asthma was higher in children who started day care center attendance during the first 2 years of life. CONCLUSIONS: Attendance to day care centers increases the risk of upper respiratory symptoms and infections in 3- to 5-year-old children. The starting age seems to be an important determinant of recurrent otitis media as well as asthma. The effect of day care center attendance on asthma is limited to age up to 2 years. This effect is most likely mediated via early respiratory tract infections that are substantially more common in children in day care centers compared with children in home care.
Chlorination of water rich in organic material is known to produce a complex mixture of organochlorine compounds, including mutagenic and carcinogenic substances. A historical cohort study of 621,431 persons living in 56 towns in Finland was conducted in order to assess the relation between historical exposure to drinking water mutagenicity and cancer. Exposure to quantity of mutagenicity was calculated on the basis of historical information of raw water quality and water treatment practices using an empirical equation relating mutagenicity and raw water pH, KMnO4 value and chlorine dose. Cancer cases were derived from the population-based Finnish Cancer Registry and follow-up time in the study started in 1970. Age, gender, time period, social class, and urban residence were taken into account in Poisson regression analysis of the observed numbers of cases using expected numbers of cases standardized for age and gender as a basis. Excess risks were calculated using a continuous variable for mutagenicity for 3,000 net rev/l exposure representing an average exposure in a town using chlorinated surface water. After adjustment for confounding, a statistically significant excess risk was observed for women in cancers of the bladder (relative risk [RR] = 1.48, 95 percent confidence interval [CI] = 1.01-2.18), rectum (RR = 1.38, CI = 1.03-1.85), esophagus (RR = 1.90, CI = 1.02-3.52), and breast (RR = 1.11, CI = 1.01-1.22). These results support the magnitude of excess risks for rectal and bladder cancers found in earlier epidemiologic studies on chlorination by-products and give additional information on exposure-response concerning the mutagenic compounds. Nevertheless, due to the public health importance of water chlorination, uncertainty related to the magnitude of observed risks, and the fact that excess risks were observed only for women, the results of the study should be interpreted with caution.
The purpose of this study was to investigate the relationship between exposure to mutagenic drinking water and cancers of the gastrointestinal and urinary tract.
Past exposure to drinking water mutagenicity was assessed in 56 Finnish municipalities for the years 1955 and 1970. The cases of bladder, kidney, stomach, colon, and rectum cancers were derived from two periods (1967 to 1976 and 1977 to 1986). Age, sex, social class, urban living, and time period were taken into account in the Poisson regression analysis.
Statistically significant exposure-response association was observed between exposure and incidence of bladder, kidney, and stomach cancers. In an ordinary municipality using chlorinated surface water, this exposure would indicate a relative risk of 1.2 for bladder cancer and of 1.2 to 1.4 for kidney cancer compared with municipalities where nonmutagenic drinking water was consumed.
The acidic mutagenic compounds present in drinking water may play a role in the etiology of kidney and bladder cancers, but, because the results are based on aggregate data, they should be interpreted with caution.
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The detection of mutagenic and carcinogenic chlorination by-products in chlorinated drinking water has raised concern in many countries over the potential health effects of long-term exposure to these products. The relation between estimated exposure to historical drinking water mutagenicity and cancer was studied in Finland by using a population-based case-control study comprising 732 bladder cancer cases, 703 kidney cancer cases, and 914 controls. The cases were obtained from the nationwide Finnish Cancer Registry for the years 1991-1992. The controls, frequency matched by age and sex, were randomly selected from the national population registry. Information on past drinking water sources and confounding factors was acquired through a questionnaire. Historical exposure to drinking water mutagenicity was estimated by using information on past residence, past water source, and historical data on water quality and treatment. Odds ratios were calculated for an increase of 3,000 net revertants per liter (net rev/liter) in average exposure from 1950 to 1987, adjusting for age, sex, socioeconomic status, and smoking in logistic regression models. A small, statistically significant, exposure-related excess risk was found for kidney cancer for men (odds ratio = 1.49, 95 percent confidence interval (CI) 1.05-2.13) for 3,000 net rev/liter exposure level. For women, the association remained nonsignificant, with a lower odds ratio of 1.08 (95% CI 0.69-1.68). For bladder cancer, the odds ratio for both men and women was 1.22 (95% CI 0.92-1.62) for 3,000 net rev/liter exposure. However, a higher odds ratio of 2.59 (95% CI 1.13-5.94) for 3,000 net rev/liter exposure was observed for male nonsmokers.
The assessment of past exposure is a prerequisite to all epidemiological studies on drinking water and cancer. In this study the past exposure assessment of drinking water carcinogenicity was done in terms of the drinking water mutagenicity estimated from historical water parameters and compared with the methods used previously in past exposure assessments in studies on drinking water and cancer. The method was applied in 56 municipalities in Finland. The comparison of different methods in past exposure assessment suggests some advantages for the method presented as it allows a quantitative exposure assessment based on historical information on drinking water mutagenicity. Nevertheless the relevance of the method is with respect to the role of mutagenicity in carcinogenicity and the water type in question.
The purpose of the present study is to assess the relationship between early acute otitis media (AOM) and exposure to respiratory pathogens mediated by siblings and day-care. A prospective cohort of 3,754 Norwegian children born in 1992-93 was followed from birth through 12 months. One or more episodes of AOM had been experienced by 25% of the children before age one. Logistic regression analysis showed that siblings attending day-care is the most important risk factor for early AOM (ORadj = 1.9 (1.4-2.3)). The total number of children in the day-care setting is another determinant for early AOM (ORadj = 2.0 (1.4-2.6) in groups of 4 or more other children and ORadj = 1.3 (1.0-1.7) in groups of 1-3 other children as compared with those who are cared for alone). Siblings who attend day-care and the number of children in the child's own day-care setting are the most important determinants for AOM the first year of life.
The evidence of an association between passive smoking and occurrence of respiratory symptoms is relatively strong in children, whereas studies conducted in adult populations have provided inconsistent results. The objective of the present study was to examine the relations between exposure to environmental tobacco smoke (ETS) and development of respiratory symptoms in young adults during a study period of 8 years, with emphasis on the evaluation of potential dose-response pattern of the relations. The study population consisted of 117 "never smokers," who were 15 to 40 years of age at the time of initial examination, when they answered a standardized questionnaire on respiratory health, and who were reexamined 8 years later. ETS exposure at home and at work during the study period was recorded at the 8-year examination with a structured questionnaire. The symptoms studied as outcomes included wheezing, dyspnea, cough, and phlegm production. The relations between ETS exposure and development of respiratory symptoms were studied in multivariate logistic regression models controlling for age, gender, atopy, and the presence of other respiratory symptoms. Cumulative incidences of the respiratory symptoms, except of phlegm production, were consistently greater among subjects exposed to ETS compared with the reference group. A significant dose-related increase in the risk of developing dyspnea was observed in relation to ETS exposure, with an OR of 2.37 for an average exposure of 10 cigarettes/day (95% confidence interval, 1.25-4.51). The risk of developing other respiratory symptoms, apart from phlegm, was also related to ETS exposure, but these relations did not achieve statistical significance. The results provide evidence of adverse respiratory effects of ETS exposure in the home and office work environments in young adults. These findings emphasize the need for effective measures in the prevention of involuntary smoking during young adulthood.
A controlled study was conducted to evaluate the effects of a low-intensity population-based smoking cessation programme in maternity care clinics. Quitting smoking during pregnancy was assessed by a self-administered questionnaire and verified by hair nicotine concentration. In the intervention area, 58/306 women (19.0%) reported quitting smoking during pregnancy whereas in the reference area the numbers were 22/152 (14.5%) (difference = 4.5%, 95% confidence interval: -2.6%-11.6%). The intervention group indicated that they received more information on adverse effects of smoking, studied the material more actively, and felt that material from maternity care influenced their smoking behaviour more than the reference group.
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.
BACKGROUND: It is still unclear how early-life exposure to pets is related to children's risk of developing atopy-related diseases. We estimated associations between early-life exposure to pets and atopy-related diseases at 0-4 years of life in a cohort of Norwegian children. METHODS: A population-based cohort of 2531 children born in Oslo, Norway, was followed from birth to the age of 4 years. Information on early-life exposure to pets, a number of possible confounders, and atopy-related diseases was mainly collected by questionnaire. RESULTS: In logistic regression analysis adjusting for potential confounders, the odds ratio for being exposed to pets in early life (reference category: not exposed) was, for bronchial obstruction at 0-2 years of life, 1.2 (95% confidence interval 0.9, 1.8); for asthma at the age of 4 years, 0.7 (0.5, 1.1); for allergic rhinitis at the age of 4 years, 0.6 (0.4, 1.0); and for atopic eczema at 0-6 months of life, 0.7 (0.5, 0.9). CONCLUSIONS: The results indicate that early-life exposure to pets or lifestyle factors associated with exposure to pets reduce the risk of developing atopy-related diseases in early childhood. However, these findings might also be explained by selection for keeping pets.
We assessed the effects of prenatal exposure to environmental tobacco smoke on fetal growth and length of gestation. The study population consisted of 389 nonsmoking women who were selected from a population-based study in southeast Finland on the basis of questionnaire information after delivery (response rate 94%). The final exposure assessment was based on nicotine concentration of maternal hair sampled after the delivery, which measures exposure during the past 2 months (i.e., the third trimester). The exposure categories were defined a priori as high (nicotine concentration [Greater and equal to] 4.00 microg/g; n = 52), medium (0.75 to
OBJECTIVE: To assess the effect of exposure to chlorination byproducts during pregnancy on foetal growth and duration of pregnancy. METHODS: A population based study was conducted of 137,145 Norwegian children born alive in 1993--5. Information was obtained from the Norwegian medical birth registry, waterwork registry, and social science data service. The outcomes of interest were birth weight, low birth weight (
The objective of our study was to assess the occurrence of respiratory symptoms in relation to dampness and molds in dwellings in pre-school children. A population-based cross-sectional study was carried out by mailing a parent-administered questionnaire to a random sample of children in a source population consisting of all children aged 1 to 6 years of Espoo, an urban-suburban city (pop. 170,000) in the Helsinki metropolitan area. The study population included a total of 2568 children whose parents filled the questionnaire (response rate 80%). Included were questions on respiratory health, partly modified from ATS-DLD-78-C questionnaire, and potential personal and environmental determinants of the outcome. The determinants of interest were histories of water damage, presence of moisture and visible molds and perceived mold odor at home. The outcomes included persistent cough, phlegm and wheezing, persistent nasal congestion and excretion during the past 12 months and current asthma. The determinant-outcome relations were estimated in the logistic regression controlling for age, gender, parents' education, single parent or guardian, environmental tobacco smoke, gas cooking, pets and type of day care. The occurrence of persistent cough (OR 2.17; 95% CI 1.39, 3.39), phlegm (2.20; 1.27, 3.82), wheezing (2.62; 1.39, 4.39), nasal congestion (1.94; 1.15, 4.98), and nasal excretion (1.43; 0.95, 2.17) during the past year were higher with the presence of any determinant, but the occurrence of asthma (OR 1.10; 0.54, 2.24) was similar compared to the reference group. Mold odor during the past year (ORs from 2.38 to 6.87) and water damage over a year ago (ORs from 2.54 to 8.67) had the strongest association with the respiratory symptoms. A dose-response relation of the occurrence of the symptoms associated with the frequency of days with mold odor was observed. There was also a compatible time sequence between water damage taking place more than a year ago and the occurrence of symptoms during the past year. The results provide further evidence on the importance of home dampness and molds in the etiology of respiratory symptoms and new information on the role of mold odor as a risk indicator.
A hazardous-waste-treatment plant that housed an incinerator began operation in 1984, before which a baseline survey of the surrounding population and environment was conducted; 10 y later, investigators studied the same subjects. Researchers focused on mercury exposure because mercury concentrations were present in the stack emissions, and environmental monitoring revealed mercury concentrations near the plant. In 1984 and 1994 the median hair mercury concentrations were 0.5 mg/kg and 0.8 mg/kg, respectively. During the 10-y period, median hair total mercury concentrations increased by 0.35 mg/kg in workers (n = 11); by 0.16 mg/kg, 0.13 mg/kg, and 0.03 mg/kg in individuals who lived 2 km (n = 45), 2-4 km (n = 38), and 5 km (n = 30) from the plant, respectively; and by 0.02 mg/kg in the reference group (n = 55). In summary, mercury exposure increased as distance from the plant decreased; however, the increase in exposure was minimal and, on the basis of current knowledge, did not pose a health risk.
Concentrations of 17 toxic 2,3,7,8-chlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and of 36 polychlorinated biphenyl congeners (PCBs) were analyzed from 167 randomly sampled human milk samples from Southern (77 samples) and Eastern (90) Finland. The level of PCDD/Fs and PCBs in human milk in Southern Finland was about 25% higher than those from Eastern Finland. The level of PCDD/Fs in human milk in Finland was the same as in Sweden, 30-50% lower than in milk from Central Europe but about 45% higher than values from Norway or Russia. The PCB concentrations in Southern Finland were at the same level as in the Netherlands, and in Eastern Finland at the same level as in Norway. The levels of PCDD/Fs and PCBs decreased with increasing number of children: the third child was exposed to about 70% of the amount of PCDD/Fs and PCBs as compared with the first child, and the eighth to tenth child to about 20%. The congener patterns of PCDD/Fs and PCBs in Finnish human milk were similar to the countries of Central Europe, however, the levels of penta- and heptachlorinated furans were slightly higher than in milk from other countries.
The purpose of this study was to examine the relation between development of respiratory symptoms and the rate of change in ventilatory lung function in young adults during a study period of 8 yr. The study population consisted of 391 subjects who were 15 to 40 yr of age at initial examination, when they underwent spirometry and an interviewer-administered ATS-DLD-78-A questionnaire on respiratory health, and who were reexamined 8 yr later. The association between the development of symptoms and the rate of change in FEV1 over time (delta FEV1, ml/yr) was studied in a linear regression model that included the potential confounders and other determinants of the outcome. The presence of modification by such factors as smoking, childhood exposure to environmental tobacco smoke, gender, or atopy was assessed by the significance of interaction terms between potential modifiers and incident symptoms. Subjects who developed wheezing and dyspnea and in whom a doctor diagnosed asthma had a significantly greater average annual change in FEV1 compared with those without respiratory symptoms or asthma (-12.3 ml/yr, SE 5.0; -16.2 ml/yr, SE 5.5; and -42.6 ml/yr, SE 11.5, respectively). When focusing on subjects without a diagnosis of asthma, the associations with appearance of wheezing and dyspnea remained significant. The associations were in general stronger in never smokers compared with smokers and were strongest in ex-smokers. The presence of atopy was a significant modifier, so that in subjects with atopy there was a stronger negative association between the onset of cough and asthma and delta FEV1 than in those without.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Events occurring during fetal life may affect the development of the immune and respiratory systems and increase the risk of asthma and allergic diseases. OBJECTIVES: We sought to elaborate the relations between the occurrence of pregnancy complications and other pregnancy-related conditions and the risk of bronchial obstruction during the first 2 years of life and the occurrence of asthma and allergic rhinitis by the age of 4 years. Pregnancy complications were considered both as predictors of the health outcomes and as possible effects caused by other prenatal factors. METHODS: A population-based, 4-year, cohort study was carried out involving 2531 children born in Oslo, Norway. We collected information on maternally related (hyperemesis, hypertension, and preeclampsia) and uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus) and the child's health and environmental exposures at birth and at 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 and allergic rhinitis at the age of 4 years. RESULTS: In a logistic regression analysis adjusting for potential confounders, uterus-related, but not other pregnancy-related, complications increased the risk of bronchial obstruction (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.3-3.4), asthma (OR, 3.0; 95% CI, 1.8-5.4), and allergic rhinitis (OR, 2.9; 95% CI, 1.6-5.2). These relations were similar in children of atopic and nonatopic parents. CONCLUSIONS: Uterus-related complications in pregnancy increase the risk of having asthma and allergic rhinitis in childhood.