Self-rated health among Mayan women participating in a randomised intervention trial reducing indoor air pollution in Guatemala

<p>Abstract</p> <p>Background</p> <p>Indoor air pollution (IAP) from solid fuels is a serious health problem in low-income countries that can be alleviated using improved stoves. Although women are the principal users, few studies have investigated the self-assessed impact of the stoves on their health and lives.</p> <p>Methods</p> <p>This study was conducted in rural highland Guatemala, involving 89 intervention and 80 control Mayan Indian young women (mean 27.8 years, SD 7.2). Outcomes were assessed after approximately 18 months use of the new stove. Our objectives were to compare self-rated health and change in health among women participating in a randomised control trial comparing a chimney stove with an open fire, to describe impacts on women's daily lives and their perceptions of how reduced kitchen smoke affects their own and their children's health.</p> <p>Results</p> <p>On intention-to-treat analysis, 52.8% of intervention women reported improvement in health, compared to 23.8% of control women (p < 0.001). Among 84 intervention women who reported reduced kitchen smoke as an important change, 88% linked this to improvement in their own health, particularly for non-respiratory symptoms (for example eye discomfort, headache); 57% linked reduced smoke to improvement in their children's health, particularly sore eyes.</p> <p>Conclusion</p> <p>Women's perception of their health was improved, but although smoke reduction was valued, this was linked mainly with alleviation of non-respiratory symptoms like eye discomfort and headache. More focus on such symptoms may help in promoting demand for improved stoves and cleaner fuels, but education about more severe consequences of IAP exposure is also required.</p

Sickness behaviour pushed too far – the basis of the syndrome seen in severe protozoal, bacterial and viral diseases and post-trauma

Certain distinctive components of the severe systemic inflammatory syndrome are now well-recognized to be common to malaria, sepsis, viral infections, and post-trauma illness. While their connection with cytokines has been appreciated for some time, the constellation of changes that comprise the syndrome has simply been accepted as an empirical observation, with no theory to explain why they should coexist. New data on the effects of the main pro-inflammatory cytokines on the genetic control of sickness behaviour can be extended to provide a rationale for why this syndrome contains many of its accustomed components, such as reversible encephalopathy, gene silencing, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia. It is thus proposed that the pattern of pathology that comprises much of the systemic inflammatory syndrome occurs when one of the usually advantageous roles of pro-inflammatory cytokines – generating sickness behaviour by moderately repressing genes (Dbp, Tef, Hlf, Per1, Per2 and Per3, and the nuclear receptor Rev-erbα) that control circadian rhythm – becomes excessive. Although reversible encephalopathy and gene silencing are severe events with potentially fatal consequences, they can be viewed as having survival advantages through lowering energy demand. In contrast, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia may best be viewed as unfortunate consequences of extreme repression of these same genetic controls when the pro-inflammatory cytokines that cause sickness behaviour are produced excessively. As well as casting a new light on the previously unrationalized coexistence of these aspects of systemic inflammatory diseases, this concept is consistent with the case for a primary role for inflammatory cytokines in their pathogenesis across this range of diseases