Is the smokers exposure to environmental tobacco smoke negligible?

Background  

Very few studies have evaluated the adverse effect of passive smoking exposure among active smokers, probably due to the unproven assumption that the dose of toxic compounds that a smoker inhales by passive smoke is negligible compared to the dose inhaled by active smoke.     

Does perceived safety of light cigarette encourage smokers to smoke more or to inhale more deeply?

OBJECTIVES: This study investigated the effect of smoking light cigarettes and believing that light cigarettes are less of a health threat on the decision to smoke more light cigarettes or inhale more deeply in Taiwan. METHODS: Demographic and smoking characteristic data for 1,182 smokers who believe that smoking light cigarettes is relatively safe was obtained from the 2002 Survey of the Health Promotion Knowledge, Attitudes, and Behavior of Taiwan Citizens; this data was used to establish Logit models for the decision to smoke more light cigarettes or inhale more deeply. RESULTS: Respectively 5.64% and 4.76% of the light cigarette smokers were motivated to smoke more light cigarettes or inhale more deeply by their belief that light cigarettes are relatively safe. Light cigarette smokers, who believe that light cigarettes are relatively safe and who wish to quit smoking, and light smokers, are both likely to smoke more light cigarettes or inhale light cigarettes more deeply in comparison to ordinary cigarette smokers. CONCLUSIONS: Government should attempt to reverse the tendency for light smokers to smoke more under the misconception that light cigarettes are relatively safe, and correct the erroneous belief among smokers who wish to quit that smoking light cigarettes is an intermediate stage on the path to quitting.     

Does suggestibility modify acute reactions to passive cigarette smoke exposure?

The influence of suggestibility on responses to passive cigarette smoke exposure was tested in a group of 24 healthy adult nonasthmatic nonsmokers and 16 asthmatic nonsmokers. Sixty-five-min exposures to air and to moderate (17 ppm carbon monoxide) and heavy (31 ppm carbon monoxide) concentrations of machine-produced cigarette smoke were carried out according to a design that permitted all six permutations of the three treatments to be equally represented. Nonasthmatic subjects exercised intermittently at an intensity inducing a respiratory ventilation of 43.6 liters/min, while asthmatic individuals were at rest, in a 14.6-m3 chamber; all viewed a bank of burning cigarettes during each exposure. Significant dose-response relationships were observed for reported symptoms, deterioration of pulmonary function, increase in nasal airflow resistance, and increase of carboxyhemoglobin levels. These findings could reflect either a pure physiological response, or an interaction between physiological and psychological responses. For asthmatics, correlations between pulmonary function responses and baseline measures of suggestibility showed 5/45 (11%) significant correlations (P less than 0.05) for both the ratio of saline diluent/air FEV1 during methacholine inhalation challenge and an index derived from the Minnesota Multiphasic Personality Inventory (MMPI), while no significant correlations were shown with the James "locus of control" test. Nonasthmatics showed 4/45 (9%) significant correlations for both the James test and the MMPI index, and 1/45 (2%) for the ratio of saline diluent/air FEV1. It is concluded that while suggestibility may augment physiological responses to passive smoking, any effect is relatively weak.     

Is it time to reassess the categorization of disease burdens in low-income countries?

The classification of disease burdens is an important topic that receives little attention or debate. One common classification scheme, the broad cause grouping, is based on etiology and health transition theory and is mainly concerned with distinguishing communicable from noncommunicable diseases. This may be of limited utility to policymakers and planners. We propose a broad care needs framework to complement the broad cause grouping. This alternative scheme may be of equal or greater value to planners. We apply these schemes to disability-adjusted life year estimates for 2000 and to mortality data from Tanzania. The results suggest that a broad care needs approach could shift the priorities of health planners and policymakers and deserves further evaluation.     

The meningococcal antibody test: how useful in the diagnosis of meningococcal disease?

Based on 9257 [correction] blood samples received from 7365 patients with a request for a meningococcal antibody test (MAT) during a 10-year period (1986-1995), the usefulness of the test in the diagnosis of meningococcal disease was assessed. Of 635 patients with culture-confirmed meningococcal disease, 88% were seronegative on admittance to hospital and 90% were seropositive 10-15 days after onset of disease. The humoral immune response in children <2 years of age was weaker than in older children and adults. Among 893 MAT-positive patients without culture-confirmed meningococcal disease, 261 (29%) had been notified as cases of meningococcal disease. Among 228 patients notified as serologically confirmed the MAT results were consistent with the clinical diagnosis in 86%. MAT is a reliable tool for establishing a diagnosis in patients with suspected meningococcal disease. Key factors facilitating appropriate interpretation of negative as well as positive test results were: time(s) of sampling(s) after onset of disease, age of the patient and clinical features.     

Is it time for the sociology of health to abandon ‘risk’?

‘Risk’ has been a fruitful seam for sociological enquiry about health and illness, generating theoretical understanding of the links between cultural analysis of modernity and the ways in which individuals makes sense of, and act in the face of, threats to their health. However, as both a topic area of research and a way of framing our understanding of how people deal with uncertainty and misfortune, it has become what could be called a ‘second order’ object of enquiry: we are no longer interested in risk per se (how it is managed, perceived, utilised) but in which domains it may be salient, or what the implications are of particular discursive evocations of ‘risk’. Drawing on empirical work in the areas of food safety and road safety, this paper identifies some limitations of locating research within the field of risk. It may be time for the sociology of health and illness to abandon an over-reliance on theoretical accounts of risk for framing empirical studies.     

Did it fall or was it pushed? The contribution of trends in established risk factors to the decline in premature coronary heart disease mortality in New Zealand

OBJECTIVE: To estimate the contribution of trends in three risk factors--systolic blood pressure (SBP), total blood cholesterol (TBC) and cigarette smoking--to the decline in premature coronary heart disease (CHD) mortality in New Zealand from 1980-2004. METHOD: Risk factor prevalence data by 10-year age group (35-64 years) and sex was sourced from six national or Auckland regional health surveys and three population censuses (the latter only for smoking). The data were smoothed using two-point moving averages, then further smoothed by fitting quadratic regression equations (SBP and TBC) or splines (smoking). Risk factor/CHD mortality hazard ratios estimated by expert working groups for the World Health Organization Global Burden of Disease Study 2001 were used to translate average annual changes in risk factor prevalences to the corresponding percentage changes in premature CHD mortality. The expected trends in CHD mortality were then compared with the observed trend to estimate the contribution of each risk factor to the decline. FINDINGS: Approximately 80% (73% for males, 87% for females) of the decline in premature CHD mortality from 1980 to 2004 is estimated to have resulted from the joint trends in population SBP and TBC distributions and smoking prevalence. Overall, approximately 42%, 36% and 22% of the joint risk factor effect was contributed by trends in SBP, TBC and smoking respectively. CONCLUSION: Our estimate for the joint risk factor contribution to the CHD mortality decline of 80% exceeds those of two earlier New Zealand studies, but agrees closely with a similar Australian study. This provides an indicator of the scope that still remains for further reduction in CHD mortality through primary and secondary prevention.     

Is it wise to restrict fat in the diets of children?

The proponents of fat-restricted diets for children argue that low-fat diets given in childhood will prevent the development of atherosclerosis in adulthood, low-fat diets given a childhood will condition children to prefer low-fat diets in adulthood, and low-fat diets for children are safe. There is no evidence that low-fat diets in childhood will prevent atherosclerosis in adulthood. In fact, studies of migrating populations indicate that immigrants to the United States from Third World countries who consumed low-fat diets in childhood take on the character of their new environments, including higher serum cholesterol levels and more coronary disease. The prevalence of fatty streaks in childhood bears little relationship to the prevalence of atheromatous plaques in adulthood. In fact, girls have more aortic fatty streaks and higher serum cholesterol values in childhood than boys, but fewer plaques in adulthood and less coronary disease. From the PDAY study, it has also been learned that hypercholesterolemia in childhood enhances fatty streak formation, but not that of plaques. It now seems established from autopsy studies that the progression of atherosclerosis from fatty streaks to plaque is arrested in childhood and does not begin to a significant extent until after puberty in males and after menopause in females. So the oft-repeated statement that atherosclerosis begins in childhood is semantically true but very misleading. The particularly harmful form of atherosclerosis (the plaque) does not become significant until much beyond puberty. The effects of low-fat, low-cholesterol diets on serum lipids and lipoproteins are of a lesser magnitude in children than in adults. The 0.78 mmol/L decrease in LDL cholesterol in the intervention group from controls (change 1.5%) in the DISC study was biologically insignificant and reflects the tighter control of lipoprotein and cholesterol synthesis in children compared with adults. It must be remembered that the human body synthesizes all of the cholesterol it needs from acetyl CoA. In general, the larger the amount of dietary cholesterol absorbed, the smaller the rate of biosynthesis of cholesterol. In some adults and most children this homeostatic control is nearly perfect, but in many adults the correction in biosynthesis of cholesterol with increased dietary input is imperfect and LDL cholesterol values increase. The second argument of the proponents of low-fat diets for children is that they are conditioned to continue low-fat diets in adulthood. From the studies of Birch and Fisher (51) this prediction seems unlikely. These investigators found that restricting access to palatable foods enhanced the interest of 3- to 5-year-old children in those foods and increased their desire to obtain and consume those foods. They concluded that "stringent parental controls can potentiate preference for high-fat energy-dense foods, limit children's acceptance of a variety of foods and disrupt children's regulation of energy intake." Brosin (52) has also observed that food restriction in childhood may lead to gluttony in adulthood. Finally, the claim that low-fat diets are safe in childhood is based on observations over too short a time to establish safety. It is true that growth and development of children studied in the DISC study was not changed from the expected increments, but that is not proof of long-term safety. In addition, the lower content of essential nutrients in low-fat, low-cholesterol diets (calcium, zinc, magnesium, phosphorus, vitamin E, vitamin B-12, thiamin, niacin, and riboflavin) must be considered along-term risk (53,54). Furthermore, the published studies of the safety of low-fat diets have been conducted under intensive surveillance in medical centers, conditions very different from those in the homes of free-living families.     

Ultraviolet exposure in childhood and in adulthood: which life period modifies the risk of melanoma more substantially?

The paper is devoted to the analysis of the relationship between the frequency of sunburns in childhood and adulthood, respectively, and the occurrence of malignant melanoma of the skin. The analysis is based on case-control data of 603 melanoma cases and 627 population controls from 11 participating centers in seven European countries. The results confirm the increase in melanoma risk for an increasing number of sunburns during childhood and adulthood in the same magnitude of risk elevation. The maximum OR for the highest exposure category of more than five sunburns was during the childhood 2.0 (95%-CI: 1.2-3.5) and during the adulthood 2.1 (95%-CI: 1.4-3.3), respectively. The analysis of the joint effects of sunburns during child- and adulthood on melanoma development corroborated these findings. In this joint analysis an OR of 2.1 (95%-CI: 1.3-3.5) quantifies the melanoma risk of those with three or more sunburns during child- and adulthood, respectively, compared to those without any sunburns during these periods. The study does therefore provide no supporting evidence for the presence of "critical period" during childhood in which a higher melanoma risk due to sunburns has been suggested by other studies.     

Does arsenic exposure increase the risk for circulatory disease?

Studies of residents in communities with high endemic concentrations of arsenic in drinking water suggest a deleterious effect on the circulatory system; however, studies among workers with high occupational exposures generally have shown either no or weak associations. This discrepancy could be a result of the healthy worker effect, including the healthy hire component and the healthy worker survivor effect (HWSE). Therefore, the authors conducted analyses of arsenic exposure in relation to circulatory disease mortality among 2,802 Tacoma, Washington, smelter workers by using 1) internal comparisons to control for the healthy hire effect and 2) the lagging method, adjustment for employment status, and the G-null test to control for the HWSE. Both lagging and adjustment for work status increased circulatory mortality rate ratios at all exposure levels, as compared with a baseline Poisson model. This excess mortality was limited to cardiovascular disease; no excess was observed for cerebrovascular disease. G-null analyses suggested no adverse effect, but power was very limited for this analysis. Overall, these results may indicate that the HWSE obscures an effect of arsenic on circulatory disease. Since cardiovascular deaths constitute about one-third of total mortality, small rate ratios translate into large numbers of excess deaths and, if causal, could be of wide public health significance. Further studies of arsenic exposure and cardiovascular disease are needed, and those conducted in occupational cohorts must control for the HWSE.     

Attributable mortality to radon exposure in Galicia,Spain. Is it necessary to act in the face of this health problem?

Background  

Radon is the second risk factor for lung cancer after tobacco consumption and therefore it is necessary to know the burden of disease due to its exposure. The objective of this study is to estimate radon-attributable lung cancer mortality in Galicia, a high emission area located at the Northwest Spain.     

Are girls more susceptible to the effects of prenatal exposure to tobacco smoke on asthma?

BACKGROUND: Prenatal exposure to tobacco smoke through mother's smoking increases the risk of developing asthma later in life. A recent study suggested that this effect is present only in girls. We explored potential differences in susceptibility between boys and girls. METHODS: We followed all 58,841 Finnish singleton babies born in 1987 through 5 nationwide registries for 7 years and identified all cases of doctor-diagnosed asthma (ICD-9 code 493). The birth registry provided categorical information on the mother's smoking during pregnancy: no smoking (reference), low exposure (<10 cigarettes per day), and high exposure (>10 cigarettes per day). RESULTS: In girls the cumulative incidence of asthma was 0.0245 in the reference group, 0.0310 in the low maternal smoking group (risk difference = 0.0065; 95% CI = 0.0053-0.0076), and 0.0360 in the high maternal smoking group (0.0115; 0.0096-0.0133). The corresponding cumulative incidences for boys were 0.0405, 0.0501 (0.0096; 0.0089-0.0103), and 0.0522 (0.0117; 0.0091-0.0142). In logistic regression analysis adjusting for confounding, the combined effect of male sex and high maternal smoking (compared with female sex and no smoking) was 112% excess risk. This corresponded closely to what would be expected from the additive independent effects of male sex (67% excess risk) and high maternal smoking (44% excess risk). CONCLUSIONS: Effects of maternal smoking during pregnancy on the risk of developing asthma are similar in boys and girls, with no interaction on an additive scale.     

Is it feasible to construct a community profile of exposure to industrial air pollution?

OBJECTIVE—An epidemiological investigation to assess the validity of residential proximity to industry as a measure of community exposure.
METHODS—19 Housing estates in Teesside (population 1991: 77 330) in north east England were grouped into zones: A=near; B=intermediate; C=further from industry. With residential proximity of socioeconomically matched populations as a starting point a historical land use survey, historical air quality reports, air quality monitoring, dispersion modelling data, and questionnaire data, were examined.
RESULTS—The populations in zones A, B, and C were similar for socioeconomic indicators and smoking history. Areas currently closest to industry had also been closest for most of the 20th century. Historical reports highlighted the influence of industrial emissions to local air quality, but it was difficult to follow spatial pollution patterns over time. Whereas contemporary NO_x and benzene concentrations showed no geographical variation, dispersion modelling of emissions (116 industrial stacks, traffic, and domestic sources) showed a gradient associated with industry. The presumed exposure gradient of areas by proximity to industry (A>B>C) was evident for all of zone A and most of zones B and C.
CONCLUSIONS—It was feasible to assemble a picture of community exposure by integration of measurements from different sources. Proximity of residence was a reasonable surrogate for complex community exposure.


Keywords: exposure assessment; community exposure; industrial pollution     

Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer's disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease.