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Background: Exacerbations of chronic obstructive pulmonary disease (COPD) contribute greatly to increased morbidity, mortality and diminished quality of life. Recent studies report moderately strong positive associations between exposures to several air pollutants and COPD-related emergency department (ED) visits and hospital admissions (HA). Studies that use clinically defined exacerbations rather than counting ED visits and HA may be more sensitive to environmental triggers like air pollution, but very few such studies exist. Participants in a COPD disease management group living in an area of low air pollution and who were followed closely for the earliest signs of an exacerbation provided an opportunity to study associations between air pollution and COPD exacerbation. Methods: Associations between short term exposures to air pollutants, including sulfur dioxide (SO2), nitrogen dioxide (NO2), and particulate matter < 2.5 microns (PM2.5), and COPD exacerbation were assessed among 168 patients residing in central Massachusetts, a region with air pollution levels well below USEPA National Ambient Air Quality Standards (NAAQS). Case-crossover analyses and multivariate conditional logistic regression were used to estimate associations between 7-day average concentrations of each air pollutant, as measured at central site monitors, and COPD exacerbation experienced in the patients'homes during the period 2012–2013, while controlling for temperature and self-reported influenza. Results: We found that short-term exposures to SO2 were associated with an increase in COPD exacerbation risk (odds ratio (OR) = 2.45, 95 % CI: 1.75–3.45 per 1 ppb increase) after adjustment for PM2.5. Short-term exposures to NO2 concentrations showed a weaker association, (OR = 1.17, 95 % CI: 1.05–1.30 per 1 ppb increase) after adjustment for PM2.5. An unexpectedly modest negative association was seen for short-term exposures to PM2.5. Conclusions: Despite living in an area with air pollution concentrations below current USEPA NAAQS, these COPD patients appeared to suffer increased risk of COPD exacerbation following short-term exposures to increased concentrations of SO2 and NO2. An unexpected negative association with PM2.5 may result from the complex air chemistry of low level PM in this region. [ABSTRACT FROM AUTHOR]

Background: Autism and Autism Spectrum Disorder (ASD) are complex neurodevelopmental disorders. Susceptibility is believed to be the interaction of genetic heritability and environmental factors. The synchronous rises in autism/ASD prevalence and paracetamol (acetaminophen) use, as well as biologic plausibility have led to the hypothesis that paracetamol exposure may increase autism/ASD risk. Methods: To explore the relationship of antenatal paracetamol exposure to ASD, population weighted average autism prevalence rates and paracetamol usage rates were compared. To explore the relationship of early neonatal paracetamol exposure to autism/ASD, population weighted average male autism prevalence rates for all available countries and U.S. states were compared to male circumcision rates - a procedure for which paracetamol has been widely prescribed since the mid-1990s. Prevalence studies were extracted from the U.S. Centers for Disease Control and Prevention Summary of Autism/ASD Prevalence Studies database. Maternal paracetamol usage and circumcision rates were identified by searches on Pub Med. Results: Using all available country-level data (n = 8) for the period 1984 to 2005, prenatal use of paracetamol was correlated with autism/ASD prevalence (r = 0.80). For studies including boys born after 1995, there was a strong correlation between country-level (n = 9) autism/ASD prevalence in males and a country's circumcision rate (r = 0.98). A very similar pattern was seen among U.S. states and when comparing the 3 main racial/ethnic groups in the U.S. The country-level correlation between autism/ASD prevalence in males and paracetamol was considerably weaker before 1995 when the drug became widely used during circumcision. Conclusions: This ecological analysis identified country-level correlations between indicators of prenatal and perinatal paracetamol exposure and autism/ASD. State level correlation was also identified for the indicator of perinatal paracetamol exposure and autism/ASD. Like all ecological analyses, these data cannot provide strong evidence of causality. However, biologic plausibility is provided by a growing body of experimental and clinical evidence linking paracetamol metabolism to pathways shown to be important in autism and related developmental abnormalities. Taken together, these ecological findings and mechanistic evidence suggest the need for formal study of the role of paracetamol in autism. [ABSTRACT FROM AUTHOR]

The eruption of genetic research presents a tremendous opportunity to epidemiologists to improve our ability to identify causes of ill health. Epidemiologists have enthusiastically embraced the new tools of genomics and proteomics to investigate gene-environment interactions. We argue that neither the full import nor limitations of such studies can be appreciated without clarifying underlying theoretical models of interaction, etiologic fraction, and the fundamental concept of causality. We therefore explore different models of causality in the epidemiology of disease arising out of genes, environments, and the interplay between environments and genes. We begin from Rothman's "pie" model of necessary and sufficient causes, and then discuss newer approaches, which provide additional insights into multifactorial causal processes. These include directed acyclic graphs and structural equation models. Caution is urged in the application of two essential and closely related concepts found in many studies: interaction (effect modification) and the etiologic or attributable fraction. We review these concepts and present four important limitations. 1. Interaction is a fundamental characteristic of any causal process involving a series of probabilistic steps, and not a second-order phenomenon identified after first accounting for "main effects". 2. Standard methods of assessing interaction do not adequately consider the life course, and the temporal dynamics through which an individual's sufficient cause is completed. Different individuals may be at different stages of development along the path to disease, but this is not usually measurable. Thus, for example, acquired susceptibility in children can be an important source of variation. 3. A distinction must be made between individual-based and population-level models. Most epidemiologic discussions of causality fail to make this distinction. 4. At the population level, there is additional uncertainty in quantifying interaction and assigning etiologic fractions to different necessary causes because of ignorance about the components of the sufficient cause. [ABSTRACT FROM AUTHOR]

Background: Ragpickers are informal workers who collect recyclable materials to earn a small wage. Their life and working conditions are extremely difficult. We examined minor psychiatric disorders (MPD) among a cohort of ragpickers in Pelotas, a city in southern Brazil. Methods: Ragpickers were matched by sex, age, and years of schooling with a sample of nonragpickers from the same poor neighborhoods. The cross-sectional study gathered data by interview on 990 individuals in 2004. MPD were assessed using a standard self-reporting questionnaire, the SRQ-20. Results: The prevalence of MPD among ragpickers was 44.7%, higher than reported by neighborhood controls (33.6%; p < 0.001). MPD were more common among females, those of lower economic level, smokers and alcoholics. Among occupational characteristics, MPD prevalence was associated with frequent static postures, low job satisfaction and recent work accidents. Conclusion: Ragpickers more frequently report MPD than other poor workers living in the same neighborhoods, with many of the same life conditions. Improving the work lives of these precarious workers should address not only the physical hazards of their jobs but their mental and emotional health as well. [ABSTRACT FROM AUTHOR]