Standardizing effect size from linear regression models with log-transformed variables for meta-analysis

Background: Meta-analysis is very useful to summarize the effect of a treatment or a risk factor for a given disease. Often studies report results based on log-transformed variables in order to achieve the principal assumptions of a linear regression model. If this is the case for some, but not all studies, the effects need to be homogenized. Methods: We derived a set of formulae to transform absolute changes into relative ones, and vice versa, to allow including all results in a meta-analysis. We applied our procedure to all possible combinations of log-transformed independent or dependent variables. We also evaluated it in a simulation based on two variables either normally or asymmetrically distributed. Results: In all the scenarios, and based on different change criteria, the effect size estimated by the derived set of formulae was equivalent to the real effect size. To avoid biased estimates of the effect, this procedure should be used with caution in the case of independent variables with asymmetric distributions that significantly differ from the normal distribution. We illustrate an application of this procedure by an application to a meta-analysis on the potential effects on neurodevelopment in children exposed to arsenic and manganese. Conclusions: The procedure proposed has been shown to be valid and capable of expressing the effect size of a linear regression model based on different change criteria in the variables. Homogenizing the results from different studies beforehand allows them to be combined in a meta-analysis, independently of whether the transformations had been performed on the dependent and/or independent variables

Child mortality from solid-fuel use in India: a nationally-representative case-control study

Abstract Background Most households in low and middle income countries, including in India, use solid fuels (coal/coke/lignite, firewood, dung, and crop residue) for cooking and heating. Such fuels increase child mortality, chiefly from acute respiratory infection. There are, however, few direct estimates of the impact of solid fuel on child mortality in India. Methods We compared household solid fuel use in 1998 between 6790 child deaths, from all causes, in the previous year and 609 601 living children living in 1.1 million nationally-representative homes in India. Analyses were stratified by child's gender, age (neonatal, post-neonatal, 1-4 years) and colder versus warmer states. We also examined the association of solid fuel to non-fatal pneumonias. Results Solid fuel use was very common (87% in households with child deaths and 77% in households with living children). After adjustment for demographic factors and living conditions, solid-fuel use significantly increase child deaths at ages 1-4 (prevalence ratio (PR) boys: 1.30, 95%CI 1.08-1.56; girls: 1.33, 95%CI 1.12-1.58). More girls than boys died from exposure to solid fuels. Solid fuel use was also associated with non-fatal pneumonia (boys: PR 1.54 95%CI 1.01-2.35; girls: PR 1.94 95%CI 1.13-3.33). Conclusions Child mortality risks, from all causes, due to solid fuel exposure were lower than previously, but as exposure was common solid, fuel caused 6% of all deaths at ages 0-4, 20% of deaths at ages 1-4 or 128 000 child deaths in India in 2004. Solid fuel use has declined only modestly in the last decade. Aside from reducing exposure, complementary strategies such as immunization and treatment could also reduce child mortality from acute respiratory infections

Air pollution and noncommunicable diseases: a review by the Forum of International Respiratory Societies' Environmental Committee, Part 1: the damaging effects of air pollution

Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (particulate matter with an aerodynamic diameter  103 million disability-adjusted life years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe

Air pollution and noncommunicable diseases: a review by the Forum of International Respiratory Societies' Environmental Committee, Part 2: air pollution and organ systems

Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (particulate matter with an aerodynamic diameter < 2.5 μm) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented

Manganese exposure and cognitive deficits: a growing concern for manganese neurotoxicity.

This symposium comprised five oral presentations dealing with recent findings on Mn-related cognitive and motor changes from epidemiological studies across the life span. The first contribution highlighted the usefulness of functional neuroimaging of the central nervous system (CNS) to evaluate cognitive as well as motor deficits in Mn-exposed welders. The second dealt with results of two prospective studies in Mn-exposed workers or welders showing that after decrease of Mn exposure the outcome of reversibility in adverse CNS effects may differ for motor and cognitive function and, in addition the issue of plasma Mn as a reliable biomarker for Mn exposure in welders has been addressed. The third presentation showed a brief overview of the results of an ongoing study assessing the relationship between environmental airborne Mn exposure and neurological or neuropsychological effects in adult Ohio residents living near a Mn point source. The fourth paper focused on the association between blood Mn and neurodevelopment in early childhood which seems to be sensitive to both low and high Mn concentrations. The fifth contribution gave an overview of six studies indicating a negative impact of excess environmental Mn exposure from air and drinking water on children's cognitive performance, with special attention to hair Mn as a potential biomarker of exposure. These studies highlight a series of questions about Mn neurotoxicity with respect to cognitive processes, forms and routes of exposure, adequate biomarkers of exposure, gender differences, susceptibility and exposure limits with regard to age