Suicides among cancer patients in Lithuania: A population-based census-linked study

Background: This study aims to estimate suicide risk and its socio-demographic determinants among cancer patients in the country showing the highest suicide rates among developed countries. Methods: The study is based on a unique census-linked dataset based on the linkages between the records from death and cancer registers and the 2001 population census records. Standardized mortality ratios for suicide (SMRs) were calculated for patients diagnosed with cancer in Lithuania between April 6, 2001 and December 31, 2009, relative to suicide rates in the general population. Results: We found that the relative suicide risk was elevated for both males and females, with SMRs of 1.43 (95% CI 1.23–1.66) and 1.32 (95% CI 0.95–1.80), respectively. This relationship for females became statistically significant and stronger after excluding skin cancers. The highest suicide risks were observed at older ages and during the period shortly after the diagnosis. The groups showing an increased suicide risk include lower educated, non-married, and rural male patients. Conclusion: The results of our study point to inadequacies of the health care system in dealing with mental health problems of cancer patients. Interventions allowing early detection of depression or suicidal ideation may help to prevent suicide among cancer patients in Lithuania.     

Homogeneity/Heterogeneity Hypotheses for Standardized Mortality Ratios Based on Minimum Power‐divergence Estimators

This paper analyzes the power divergence estimators when homogeneity/heterogeneity hypotheses among standardized mortality ratios (SMRs) are taken into account. A Monte Carlo study shows that when the standard mortality rate is not external, that is it is estimated from the sample data, these estimators have a good performance even for small sample sets and in particular the minimum chi‐square estimators have a better behavior compared to the classical maximum likelihood estimators. In order to make decisions under homogeneity/heterogeneity hypotheses of SMRs we propose some test‐statistics which consider the minimum power divergence estimators. Through a numerical example focused on SMRs of melanoma mortality ratios in different regions of the US, a homogeneity/heterogeneity study is illustrated.     

小反刍兽疫病毒研究进展

小反刍兽疫（PPR）是由小反刍兽疫病毒（PPRV）引起的一种主要感染小反刍动物的急性、烈性、接触性A类传染病,患病率、死亡率高。本文就世界PPR流行状况、PPRV基因组及病毒结构蛋白、PPRV检测方法、最新的药物及疫苗、存在的问题等方面做了简要综述。     

Changing temporal trends in non-AIDS cancer mortality among people diagnosed with AIDS: San Francisco,California, 1996–2013

BackgroundAntiretroviral therapy (ART) has reduced AIDS-defining cancer (ADC) mortality, but its effect on non-AIDS-defining cancer (NADC) mortality is unclear. To help inform cancer prevention and screening, we evaluated trends in NADC mortality among people with AIDS (PWA) in the ART era.MethodsThis retrospective cohort study analyzed AIDS surveillance data, including causes of death from death certificates, for PWA in San Francisco who died in 1996–2013. Proportional mortality ratios (PMRs), and year, age, race, sex-adjusted standardized mortality ratios (SMRs) were calculated for 1996–1999, 2000–2005, and 2006–2013, corresponding to advances in ART.ResultsThe study included 5822 deceased PWA of whom 90% were male and 68% were aged 35–54 at time of death. Over time, the PMRs significantly decreased for ADCs (2.6%, 1.4%, 1.2%) and increased for NADCs (4.3%, 7.0%, 12.3%). For all years combined (1996–2013) and compared to the California population, significantly elevated SMRs were observed for these cancers: all NADCs combined (2.1), anal (58.4), Hodgkin lymphoma (10.5), liver (5.2), lung/larynx (3.0), rectal (5.2), and tongue (4.7). Over time, the SMRs for liver cancer (SMR 19.8, 11.2, 5.0) significantly decreased while the SMRs remained significantly elevated over population levels for anal (SMR 123, 48.2, 45.5), liver (SMR 19.8, 11.2, 5.0), and lung/larynx cancer (SMR 5.3, 4.7, 3.6).ConclusionA decline in ADC PMRs and increase in NADC PMRs represent a shift in the cancer burden, likely due to ART use. Moreover, given their elevated SMRs, anal, liver, and lung/larynx cancer remain targets for improved cancer prevention, screening, and treatment.     

Joint Effects of Smoking and Silicosis on Diseases to the Lungs

Smokers are subject to being more susceptible to the long-term effects of silica dust, whilst it remains unclear whether the joint effect of smoking and silicosis differs amongst diseases to the lungs; this study aims to address this knowledge gap. This was a historical cohort study comprised of 3202 silicotics in Hong Kong during 1981–2005 who were followed up till 31/12/2006. We estimated the standardized mortality ratio (SMR) in the smoking and never smoking silicotics using the mortality rates of male general population indiscriminately by smoking status, but these SMRs were regarded as biased. We adjusted these biased SMRs using “smoking adjustment factors (SAF)”. We assessed the multiplicative interaction between smoking and silicosis using ‘relative silicosis effect (RSE)’ that was the ratio of SAF-corrected SMR of smoking silicotics to the never smokers. A RSE differs significantly from one implies the presence of multiplicative interaction. A significant excess SMR was observed for respiratory diseases (lung cancer, chronic obstructive pulmonary diseases [COPD], silicosis) and other diseases to the lungs (pulmonary heart disease, tuberculosis). All the ‘biased-SMRs’ in smokers were higher than those in never smokers, but the SAF-corrected SMRs became higher in never smokers. The RSE was 0.95 (95%CI: 0.37–3.55), 0.94 (95%CI: 0.42–2.60), and 0.81 (95%CI: 0.60–1.19) for lung cancer, COPD, and silicosis; whilst it was 1.21 (95%CI: 0.32–10.26) for tuberculosis and 1.02 (95%CI: 0.16–42.90) for pulmonary heart disease. This study firstly demonstrated the joint effect of smoking and silicosis may differ amongst diseases to the lungs, but power is limited.     

Estimation in Bayesian disease mapping

Recent work on Bayesian inference of disease mapping models discusses the advantages of the fully Bayesian (FB) approach over its empirical Bayes (EB) counterpart, suggesting that FB posterior standard deviations of small-area relative risks are more reflective of the uncertainty associated with the relative risk estimation than counterparts based on EB inference, since the latter fail to account for the variability in the estimation of the hyperparameters. In this article, an EB bootstrap methodology for relative risk inference with accurate parametric EB confidence intervals is developed, illustrated, and contrasted with the hyperprior Bayes. We elucidate the close connection between the EB bootstrap methodology and hyperprior Bayes, present a comparison between FB inference via hybrid Markov chain Monte Carlo and EB inference via penalized quasi-likelihood, and illustrate the ability of parametric bootstrap procedures to adjust for the undercoverage in the "naive" EB interval estimates. We discuss the important roles that FB and EB methods play in risk inference, map interpretation, and real-life applications. The work is motivated by a recent analysis of small-area infant mortality rates in the province of British Columbia in Canada.     

Joint effects of radiation and smoking on lung cancer risk among atomic bomb survivors

Results are given on the joint effect of radiation exposure and cigarette smoking on lung cancer risks among A-bomb survivors, based on 592 cases through 1994. Information on smoking was derived from mail surveys and clinical interviews of 45113 persons in the Radiation Effects Research Foundation cohort. Radiation and smoking effects on lung cancer are found to be significantly sub-multiplicative and quite consistent with additivity. The smoking relative risk, previously very low in studies of this cohort, is now similar to that found in Western populations. This increase is likely to be related to the scarcity of cigarettes during and after the war. The smoking relative risk depends little on sex. After adjusting for smoking, the radiation-related risks relative to background rates for nonsmokers are similar to those for other solid cancers: a sex-averaged ERR/Sv of about 0.9 with a female:male sex ratio of about 1.6. Adjusting for smoking removes a spuriously large female:male ratio in radiation relative risk due to confounding between sex and smoking level. The adjustment also removes an artifactual age-at-exposure effect in the radiation relative risk, opposite in direction to other cancers, which is due to birth cohort variation in lung cancer rates.     

Cigarette smoking as risk factor for late fetal and early neonatal death.

Risk factors for late fetal death and early neonatal mortality were examined in a population based prospective study. Practically all Swedish births between 1983 and 1985 were included, 281,808 births in all. The overall rates of late fetal death and early neonatal mortality were 3.5 and 3.1 per 1000, respectively. About 30% of the pregnant women were recorded as being daily smokers. Logistic regression analyses showed significant relative risks for late fetal death for high maternal age (1.4), nulliparity (1.4), multiparity (greater than or equal to 2) (1.3), smoking (1.4), and multiple births (2.8). Significant relative risks for early neonatal mortality were found for multiple births (4.9) and smoking (1.2). Smokers aged under 35 faced a relative risk of late fetal death ranging from 1.1 to 1.6, while the risk for late fetal death was doubled if the mothers were aged 35 years or more and smoked. In countries like Sweden, where maternal cigarette smoking is prevalent, smoking may be the most important preventable risk factor for late fetal death.     

Mortality patterns among industrial workers exposed to chloroprene and other substances. II. Mortality in relation to exposure

As part of an historical cohort study to investigate the mortality experience of industrial workers exposed to chloroprene (CD) and other substances, including vinyl chloride monomer (VC), we analyzed mortality from all cancers combined, respiratory system (RSC) and liver cancer in relation to CD and VC exposures. Subjects were 12,430 workers ever employed at one of two U.S. sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)). Historical exposures for individual workers were estimated quantitatively for CD and VC. For sites L, M, P and G, respectively, average intensity of CD exposures (median value of exposed workers in ppm) were 5.23, 0.16, 0.028 and 0.149 and median cumulative exposures (ppm years) were 18.35, 0.084, 0.133 and 1.01. For sites L and M, respectively, average intensity of VC exposures (median value of exposed workers in ppm) was 1.54 and 0.03 and median cumulative exposures (ppm years) were 1.54 and 0.094. We performed relative risk (RR) regression modeling to investigate the dependence of the internal cohort rates for all cancers combined, RSC and liver cancer on combinations of the categorical CD or VC exposure measures with adjustment for potential confounding factors. We categorized exposure measures into approximate quartiles based on the distribution of deaths from all cancers combined. We also considered 5- and 15-year lagged exposure measures and adjusted some RR models for worker pay type (white/blue collar) as a rough surrogate for lifetime smoking history. All modeling was site-specific to account for exposure heterogeneity. We also computed exposure category-specific standardized mortality ratios (SMRs) to assess absolute mortality rates. With the exception of a one statistically significant association with duration of exposure to CD and all cancers combined in plant M, we observed no evidence of a positive association with all cancers, RSC or liver cancer and exposure to CD and/or VC using both the unlagged and lagged exposure measures: duration, average intensity or cumulative exposure to CD or VC; time since first CD or VC exposure; and duration of CD exposure or time since first CD exposure in presence or absence of VC exposure. We observed elevated and statistically significantly elevated RRs for some analysis subgroups, but these were due to inordinately low death rates in the baseline categories. With the possible exception of all cancer mortality in plant G, our additional adjustment of RRs for pay type revealed no evidence of positive confounding by smoking. We conclude that exposures to CD or VC at the levels encountered in the four study sites do not elevate mortality risks from all cancers, RSC or liver cancer. This conclusion is corroborated by our analysis of general mortality patterns among the CD cohort reported in our companion paper [G. Marsh, A. Youk, J. Buchanich, M. Cunningham, N. Esmen, T. Hall, M. Phillips, Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns, Chem.-Biol. Interact., submitted for publication].     

The CroHort study: cardiovascular behavioral risk factors in adults, school children and adolescents, hospitalized coronary heart disease patients, and cardio rehabilitation groups in Croatia

Based on repeated measurement of health behaviors the CroHort Study showed that health behavior explains a great deal more of class inequalities in mortality than observed in previous studies. These include decreasing prevalence of smoking and increase in obesity, hypertension and diabetes mellitus. The lowest prevalence of health risks was recorded among children and adolescents, followed by general adult population from the CroHort Study. Hospitalized coronary heart disease patients had higher risks prevalence than general population, while the highest prevalence of risks was recorded among patients in cardiac rehabilitation program. The higher levels of stress were associated to lower financial conditions, poorer social functioning and poorer mental health for both men and women. Higher levels of stress were also associated with heart problems, higher alcohol consumption in men while in women stress was associated to poorer general health, higher age and lower levels of education.     

Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns

We conducted an historical cohort study to investigate the mortality experience of industrial workers potentially exposed to chloroprene (CD) and other substances, including vinyl chloride (VC), with emphasis on cancer mortality, including respiratory system (RSC) and liver. In 1999, the International Agency for Research on Cancer (IARC) classified CD as a possible carcinogen (Group 2B); VC was classified in 1987 as a known human carcinogen (Group 1). Subjects were 12,430 workers ever employed at one of two U.S. industrial sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)), with earliest CD production dates ranging from 1942 (L) to 1969 (P). Two sites (L and M) synthesized CD with the acetylene process that produced VC exposures. We determined vital status through 2000 for 95% of subjects and cause of death for 95% of the deaths. Historical exposures for individual workers were estimated quantitatively for CD and VC. Workers ever exposed to CD ranged from 92.3% (M) to 100% (G); to VC from 5.5% (M) to 22.7% (L). We computed standardized mortality ratios (SMRs) (using national and regional standard populations) in relation to selected demographic, work history and exposure factors. We used worker pay type (white or blue collar) as a rough surrogate for lifetime smoking history. For the combined cohort, SMRs (95% CIs) for all causes combined, all cancers combined, RSC and liver cancer were, respectively, 0.72 (0.69-0.74), 0.73 (0.68-0.78), 0.75 (0.67-0.84) and 0.72 (0.43-1.13). Site-specific (L, M, P and G, respectively) SMRs were: for all cancers combined: 0.75 (0.69-0.80), 0.68 (0.56-0.80), 0.68 (0.47-0.95) and 0.59 (0.36-0.91); for RSC: 0.75 (0.66-0.85), 0.79 (0.58-1.05), 0.62 (0.32-1.09) and 0.85 (0.41-1.56); for liver cancer: 0.90 (0.53-1.44) (17 deaths), 0.24 (0.01-1.34) (1 death), 0.0 (0-2.39) (no deaths) and 0.56 (0.01-3.12) (1 death). Among all workers ever exposed to CD, SMRs were: for all cancers combined: 0.71 (0.66-0.76); for RSC: 0.75 (0.67-0.84); for liver cancer: 0.71 (0.42-1.14). We also observed no increased mortality risks among cohort subgroups defined by race, gender, worker pay type, worker service type (short/long term), time period, year of hire, age at hire, duration of employment, the time since first employment, and CD or VC exposure status (never/ever exposed). In summary, our study has many strengths and is the most definitive study of the human carcinogenic potential of exposure to CD conducted to date. We conclude that persons exposed to chloroprene or vinyl chloride at the levels encountered in the four study sites did not have elevated risks of mortality from any of the causes of death examined, including all cancers combined and lung and liver cancer, the cancer sites of a priori interest. This conclusion is corroborated by our detailed analyses of mortality in relation to qualitative and quantitative exposures to CD and VC at each of the four study sites, reported in our companion paper (Marsh et al., submitted for publication).     

Cancer Mortality in Chinese Chrysotile Asbestos Miners: Exposure-Response Relationships

Objective

This study was conducted to assess the relationship of mortality from lung cancer and other selected causes to asbestos exposure levels.

Methods

A cohort of 1539 male workers from a chrysotile mine in China was followed for 26 years. Data on vital status, occupation and smoking were collected from the mine records and individual contacts. Causes and dates of death were further verified from the local death registry. Individual cumulative fibre exposures (f-yr/ml) were estimated based on converted dust measurements and working years at specific workshops. Standardized mortality ratios (SMRs) for lung cancer, gastrointestinal (GI) cancer, all cancers and nonmalignant respiratory diseases (NMRD) stratified by employment years, estimated cumulative fibre exposures, and smoking, were calculated. Poisson models were fitted to determine exposure-response relationships between estimated fibre exposures and cause-specific mortality, adjusting for age and smoking.

Results

SMRs for lung cancer increased with employment years at entry to the study, by 3.5-fold in ≥10 years and 5.3-fold in ≥20 years compared with <10 years. A similar trend was seen for NMRD. Smokers had greater mortality from all causes than nonsmokers, but the latter also had slightly increased SMR for lung cancer. No excess lung cancer mortality was observed in cumulative exposures of <20 f-yrs/ml. However, significantly increased mortality was observed in smokers at the levels of ≥20 f-yrs/ml and above, and in nonsmokers at ≥100 f-yrs/ml and above. A similarly clear gradient was also displayed for NMRD. The exposure-response relationships with lung cancer and NMRD persisted in multivariate analysis. Moreover, a clear gradient was shown in GI cancer mortality when age and smoking were adjusted for.

Conclusion

There were clear exposure-response relationships in this cohort, which imply a causal link between chrysotile asbestos exposure and lung cancer and nonmalignant respiratory diseases, and possibly to gastrointestinal cancer, at least for smokers.     

An Application of Logistic Models to the Analysis of Ordinal Responses

Logistic probability models—models linear in the log odds of the outcome event—have found extensive application in modelling of unordered categorical responses. This paper illustrates some extensions of logistic models to the modelling of probabilities of ordinal responses. The extensions arise naturally from discrete probability models for the conditional distribution of the ordinal response, as well as from linear modelling of the log odds of response. Methods of estimation and examination of fit developed for the binary logistic model extend in a straightforward manner to the ordinal models. The models and methods are illustrated in an analysis of the dependence of chronic obstructive respiratory disease prevalence on smoking and age.     

Estimating the Effects of Obesity and Weight Change on Mortality Using a Dynamic Causal Model

Background

A well-known challenge in estimating the mortality risks of obesity is reverse causality attributable to illness-associated and smoking-associated weight loss. Given that the likelihood of chronic and acute illnesses rises with age, reverse causality is most threatening to estimates derived from elderly populations.

Methods

I analyzed data from 12,523 respondents over 50 years old from a nationally representative longitudinal dataset, the Health and Retirement Study (HRS). The effects of both baseline body weight and time-varying weight change on mortality are estimated, adjusting for demographic and socio-economic variables, as well as time-varying confounders including illness and smoking. Body weight is measured by body mass index (BMI). In survival models for mortality, illness and smoking were lagged to minimize bias from reverse causality in estimates of the effect of weight change. Furthermore, because illness both causes and is caused by changes in BMI, I used a marginal structural model (MSM) rather than standard adjustment to control confounding by this and other time-dependent factors.

Results

Overall, relative to normal weight, underweight and Class II/III at baseline are associated with hazard ratios that are 2.07 (95% confidence interval (CI): 1.28–3.37) and 1.82 (1.54–2.16) respectively, whereas overweight and Class I obesity do not significantly lower or raise the mortality risks. Furthermore, relative to stable weight change, all types of weight change lead to significantly increased risk of mortality. Specifically, large weight loss results in a mortality risk that is nearly 3.86 (3.26–4.58) times of staying in the stable weight range and small weight loss is about 1.81 (1.55–2.11 ) times riskier. In contrast, large weight gain and small weight gain are associated with hazard ratios that are 1.98 (1.67–2.35) and 1.20 (1.02–1.41) respectively.

Conclusions

Being underweight or severe obese at baseline is associated with excess mortality risk, and weight change tend to raise mortality risk. Both the confounding by illness and by smoking lead to overestimates of the effects of being underweight at baseline and of weight loss, but underestimates the effect of being obese at baseline.     

Lifetime Smoking History and Cause-Specific Mortality in a Cohort Study with 43 Years of Follow-Up

BackgroundIn general, smoking increases the risk of mortality. However, it is less clear how the relative risk varies by cause of death. The exact impact of changes in smoking habits throughout life on different mortality risks is less studied.MethodsWe studied the impact of baseline and lifetime smoking habits, and duration of smoking on the risk of all-cause mortality, mortality of cardiovascular diseases (CVD), chronic obstructive pulmonary disease (COPD), any cancer and of the four most common types of cancer (lung, colorectal, prostate, and breast cancer) in a cohort study (Vlagtwedde-Vlaardingen 1965–1990, with a follow-up on mortality status until 2009, n = 8,645). We used Cox regression models adjusted for age, BMI, sex, and place of residence. Since previous studies suggested a potential effect modification of sex, we additionally stratified by sex and tested for interactions. In addition, to determine which cause of death carried the highest risk we performed competing-risk analyses on mortality due to CVD, cancer, COPD and other causes.ResultsCurrent smoking (light, moderate, and heavy cigarette smoking) and lifetime persistent smoking were associated with an increased risk of all-cause, CVD, COPD, any cancer, and lung cancer mortality. Higher numbers of pack years at baseline were associated with an increased risk of all-cause, CVD, COPD, any cancer, lung, colorectal, and prostate cancer mortality. Males who were lifetime persistent pipe/cigar smokers had a higher risk of lung cancer [HR (95% CI) = 7.72 (1.72–34.75)] as well as all-cause and any cancer mortality. A longer duration of smoking was associated with a higher risk of COPD, any and lung cancer [HR (95% CI) = 1.06 (1.00–1.12), 1.03 (1.00–1.06) and 1.10 (1.03–1.17) respectively], but not with other mortality causes. The competing risk analyses showed that ex- and current smokers had a higher risk of cancer, CVD, and COPD mortality compared to all other mortality causes. In addition, heavy smokers had a higher risk for COPD mortality compared to cancer, and CVD mortality.ConclusionOur study indicates that lifetime numbers of cigarettes smoked and the duration of smoking have different impacts for different causes of mortality. Moreover, our findings emphasize the importance of smoking-related competing risks when studying the smoking-related cancer mortality in a general population and that smoking cessation immediately effectively reduces the risk of all-cause and any cancer mortality.     

Body Mass Index and All-Cause Mortality in a Large Prospective Cohort of White and Black U.S. Adults

Remaining controversies on the association between body mass index (BMI) and mortality include the effects of smoking and prevalent disease on the association, whether overweight is associated with higher mortality rates, differences in associations by race and the optimal age at which BMI predicts mortality. To assess the relative risk (RR) of mortality by BMI in Whites and Blacks among subgroups defined by smoking, prevalent disease, and age, 891,572 White and 38,119 Black men and women provided height, weight and other information when enrolled in the Cancer Prevention Study II in 1982. Over 28 years of follow-up, there were 434,400 deaths in Whites and 18,702 deaths in Blacks. Cox proportional-hazards regression was used to estimate multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI). Smoking and prevalent disease status significantly modified the BMI-mortality relationship in Whites and Blacks; higher BMI was most strongly associated with higher risk of mortality among never smokers without prevalent disease. All levels of overweight and obesity were associated with a statistically significantly higher risk of mortality compared to the reference category (BMI 22.5–24.9 kg/m²), except among Black women where risk was elevated but not statistically significant in the lower end of overweight. Although absolute mortality rates were higher in Blacks than Whites within each BMI category, relative risks (RRs) were similar between race groups for both men and women (p-heterogeneity by race  = 0.20 for men and 0.23 for women). BMI was most strongly associated with mortality when reported before age 70 years. Results from this study demonstrate for the first time that the BMI-mortality relationship differs for men and women who smoke or have prevalent disease compared to healthy never-smokers. These findings further support recommendations for maintaining a BMI between 20–25 kg/m² for optimal health and longevity.     

Household environmental tobacco smoke and risks of asthma,wheeze and bronchitic symptoms among children in Taiwan

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.     

Risk of disability and mortality due to overweight in a Finnish population.

OBJECTIVE--To investigate the effect of overweight on premature mortality and work disability in young and middle aged Finns. DESIGN--Prospective cohort study based on data collected in the multiphasic health examinations by the Social Insurance Institution of Finland from 1966 to 1972 and follow up until 1982. SETTING--34 Communities throughout Finland. SUBJECTS--12,053 Women and 19,076 men who were employed and aged 25-64 at baseline. MAIN OUTCOME MEASURES--Mortality and work disability pensions from all and specified causes. RESULTS--Body mass index was a weak predictor of death but a strong predictor of early work disability, which increased linearly with body mass index. After adjustment for age, geographical region, occupation, and smoking the relative risks of work disability for women and men with a body mass index greater than or equal to 30 kg/m2 were, respectively, 2.0 (95% confidence interval 1.8 to 2.3) and 1.5 (1.3 to 1.7) when compared with those of subjects with body mass index less than 22.5 kg/m2. The increased risks were due to an excess of cardiovascular and musculoskeletal diseases but not of mental diseases. One fourth of all disability pensions from cardiovascular and musculoskeletal causes in women and half as many in men could be attributed to overweight (body mass index greater than 25 kg/m2) alone. CONCLUSIONS--Though modest overweight has little impact on mortality it predicts severe functional impairment. A considerable proportion of work disability pensions could probably be prevented by efficient weight control.