Smoke-free air laws and quit attempts: evidence for a moderating role of spontaneous self-affirmation

Background: In addition to their primary goal of protecting nonsmokers from secondhand smoke, smoke-free air laws may also encourage intentions to quit smoking, quit attempts, and cessation among smokers. However, laws may not encourage quitting if smokers feel threatened by them and react defensively. Objective: This study examined whether spontaneous self-affirmation - the extent to which people think about their values or strengths when they feel threatened - may reduce smokers' reactance to smoke-free laws, enhancing the ability of the laws to encourage quitting. Method: We linked state-level information on the comprehensiveness of U.S. smoke-free laws (compiled in January, 2013 by the American Lung Association) with data from a U.S. health survey (Health Information National Trends Survey) collected from September-December, 2013 (N = 345 current smokers; 587 former smokers). Results: Smoke-free laws interacted with self-affirmation to predict quit attempts in the past year and intentions to quit in the next six months: Smokers higher in self-affirmation reported more quit attempts and quit intentions if they lived in states with more comprehensive smoke-free laws. There was some evidence of a "boomerang" effect (i.e., less likelihood of making a quit attempt) among smokers low in self-affirmation if living in states with more comprehensive smoke-free laws, but this effect was significant only among smokers extremely low in self-affirmation. For quit intentions, there was no evidence for a boomerang effect of smoke-free laws even among smokers extremely low in self-affirmation. More comprehensive smoke-free laws were not associated with smoking status (former vs. current smoker) or average amount smoked per day, nor did they interact with self-affirmation to predict these outcomes. Conclusions: The impact of smoke-free policies on quit attempts and quit intentions may be moderated by psychological characteristics such as the tendency to spontaneously self-affirm. Follow-ups should experimentally manipulate self-affirmation and examine effects of smoke-free laws in controlled contexts

Why the increase in under five mortality in Uganda from 1995 to 2000? A retrospective analysis

<p>Abstract</p> <p>Background</p> <p>From 1995-2000 the under five mortality rate in Uganda increased from 147.3 to 151.5 deaths per 1000 live births and reasons for the increase were not clear. This study was undertaken to understand factors influencing the increase in under five mortality rate during 1995-2000 in Uganda with a view of suggesting remedial actions.</p> <p>Methods</p> <p>We performed a comparative retrospective analysis of data derived from the 1995 and the 2000 Uganda demographic and health surveys. We correlated the change of under five mortality rate in Uganda desegregated by region (central, eastern, north and western) with change in major known determinants of under five mortality such social economic circumstances, maternal factors, access to health services, and level of nutrition.</p> <p>Results</p> <p>The increase in under five mortality rate only happened in western Uganda with the other 3 regions of Uganda (eastern, northern and central) showing a decrease. The changes in U5MR could not be explained by changes in poverty, maternal conditions, level of nutrition, or in access to health and other social services and in the prevalence of HIV among women attending for ante-natal care. All these factors did not reach statistical significance (P > 0.05) using Pearson's correlation coefficient.</p> <p>Conclusion</p> <p>In order to explain these findings, there is need to find something that happened in western Uganda (but not other parts of the country) during the period 1995-2000 and has the potential to change the under five mortality by a big margin. We hypothesize that the increase in under five mortality could be explained by the severe malaria epidemic that occurred in western Uganda (but not other regions) in 1997/98.</p

A longitudinal survey of African animal trypanosomiasis in domestic cattle on the Jos Plateau, Nigeria:prevalence, distribution and risk factors

BACKGROUND: Trypanosomiasis is a widespread disease of livestock in Nigeria and a major constraint to the rural economy. The Jos Plateau, Nigeria was free from tsetse flies and the trypanosomes they transmit due to its high altitude and the absence of animal trypanosomiasis attracted large numbers of cattle-keeping pastoralists to inhabit the plateau. The Jos Plateau now plays a significant role in the national cattle industry, accommodating approximately 7% of the national herd and supporting 300,000 pastoralists and over one million cattle. However, during the past two decades tsetse flies have invaded the Jos Plateau and animal trypanosomiasis has become a significant problem for livestock keepers. METHODS: In 2008 a longitudinal two-stage cluster survey on the Jos Plateau. Cattle were sampled in the dry, early wet and late wet seasons. Parasite identification was undertaken using species-specific polymerase chain reactions to determine the prevalence and distribution bovine trypanosomiasis. Logistic regression was performed to determine risk factors for disease. RESULTS: The prevalence of bovine trypanosomiasis (Trypanosoma brucei brucei, Trypanosoma congolense savannah, Trypanosoma vivax) across the Jos Plateau was found to be high at 46.8% (39.0 – 54.5%) and significant, seasonal variation was observed between the dry season and the end of the wet season. T. b. brucei was observed at a prevalence of 3.2% (1% – 5.5%); T. congolense at 27.7% (21.8% - 33.6%) and T. vivax at 26.7% (18.2% - 35.3%). High individual variation was observed in trypanosomiasis prevalence between individual villages on the Plateau, ranging from 8.8% to 95.6%. Altitude was found to be a significant risk factor for trypanosomiasis whilst migration also influenced risk for animal trypanosomiasis. CONCLUSIONS: Trypanosomiasis is now endemic on the Jos Plateau showing high prevalence in cattle and is influenced by seasonality, altitude and migration practices. Attempts to successfully control animal trypanosomiasis on the Plateau will need to take into account the large variability in trypanosomiasis infection rates between villages, the influence of land use, and husbandry and management practices of the pastoralists, all of which affect the epidemiology of the disease

Linear low-dose extrapolation for noncancer health effects is the exception, not the rule

The nature of the exposure-response relationship has a profound influence on risk analyses. Several arguments have been proffered as to why all exposure-response relationships for both cancer and noncarcinogenic end-points should be assumed to be linear at low doses. We focused on three arguments that have been put forth for noncarcinogens. First, the general “additivity-to-background” argument proposes that if an agent enhances an already existing disease-causing process, then even small exposures increase disease incidence in a linear manner. This only holds if it is related to a specific mode of action that has nonuniversal properties—properties that would not be expected for most noncancer effects. Second, the “heterogeneity in the population” argument states that variations in sensitivity among members ofthe target population tend to “flatten out and linearize” the exposure-response curve, but this actually only tends to broaden, not linearize, the dose-response relationship. Third, it has been argued that a review of epidemiological evidence shows linear or no-threshold effects at low exposures in humans, despite nonlinear exposure-response in the experimental dose range in animal testing for similar endpoints. It is more likely that this is attributable to exposure measurement error rather than a true non-threshold association. Assuming that every chemical is toxic at high exposures and linear at low exposures does not comport to modern-day scientific knowledge of biology. There is no compelling evidence-based justification for a general low-exposure linearity; rather, case-specific mechanistic arguments are needed