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Since the early 1980s, there has been growing concern about potential adverse health effects related to exposure to environmental tobacco smoke (ETS). Evidence has accumulated on ill-health associated with ETS, and such exposure has now been documented among children and adults in many countries [1][2][3][4][5][6][7][8]. A major difficulty in studying the ill-health effects of ETS has been assessing exposure, since this may occur in multiple settings with highly variable concentrations and exposure profiles may vary considerably during different age periods. Accurate and precise exposure assessment is crucial, since health effects of ETS are likely to be relatively small in magnitude. Appropriate exposure assessment is also needed for inferring causality and for risk assessment. In addition, exposure assessment is obviously necessary for development of preventive strategies.The purpose of this paper is to present a theoretical framework for assessment of exposure to ETS, and to review current methods of exposure assessment in order to provide guidelines for choice of appropriate methods for different types of study. General definitions and concepts of exposure and its assessment will be presented, followed by definitions and components of ETS. The principles for assessment of ETS exposure will then be presented. Current methods of assessment will be reviewed in terms of their advantages and disadvantages, followed by a very brief summary of the ill-health effects of ETS. This allows the criteria for selection of the appropriate method of assessing ETS exposure to be set in context, and to be formulated as user guidelines. Definitions of concentration, exposure and dose ConcentrationConcentration is the amount of a contaminant at a particular location in a particular medium [9]. For example, for an air pollutant it is the amount of the material contained in a specified volume of air. Air pollutant concentrations are usually expressed as mass per unit volume, e.g. µg·m -3 , and gaseous pollutants may also be expressed as a mixing ratio with air, e.g. parts per million (ppm) by volume. Air pollutant concentrations vary in time and space. ExposureExposure is defined as the contact of pollutant with a susceptible surface of the human body [9][10][11]. For ETS, this means contact with the eyes, the epithelium of the nose, mouth and throat, and the lining of the airways and alveoli. With respect to time, there are a number of possible formulations, including instantaneous exposure, peak exposure, average exposure over a specified time period, and cumulative exposure [11]. The best approach to assess ETS exposure will depend on the aim of the study, the health outcome, and the resources. Personal monitoring of nicotine or RSPs is the best method in studies of short-term health effects with small study samples. Stationary measurements of indoor air nicotine or RSPs are suitable for overall monitoring of ETS in different microenvironments over time. Questionnaires and interviews are suitable when studying health outcomes ...

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Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.

ContextStudies from different geographical regions have assessed the relations between indoor dampness and mold problems and the risk of asthma, but the evidence has been inconclusive.ObjectiveTo assess the relations between indicators of indoor dampness and mold problems and the risk of developing new asthma, and to investigate whether such relations differ according to the type of exposure.Data sourcesA systematic literature search of PubMed database from 1990 through March 2012 and the reference lists of recent reviews and of relevant articles identified in our search.Study selectionCohort/longitudinal and incident case-control studies assessing the relation between mold/dampness and new asthma were included.Data extractionThree authors independently evaluated eligible articles and extracted relevant information using a structured form.SynthesisSixteen studies were included: 11 cohort and 5 incident case-control studies. The summary effect estimates (EE) based on the highest and lowest estimates for the relation between any exposure and onset of asthma were 1.50 (95% confidence interval [CI] 1.25–1.80, random-effects model, Q-statistic 38.74 (16), P = 0.001) and 1.31 (95% CI 1.09–1.58, random-effects model, Q-statistic 40.08 (16), P = 0.000), respectively. The summary effect estimates were significantly elevated for dampness (fixed-effects model: EE 1.33, 95% CI 1.12–1.56, Q-statistic 8.22 (9), P = 0.413), visible mold (random-effects model; EE 1.29, 95% CI 1.04–1.60, 30.30 (12), P = 0.001), and mold odor (random-effects model; EE 1.73, 95% CI 1.19–2.50, Q-statistics 14.85 (8), P = 0.038), but not for water damage (fixed-effects model; EE 1.12, 95% CI 0.98–1.27). Heterogeneity was observed in the study-specific effect estimates.ConclusionThe evidence indicates that dampness and molds in the home are determinants of developing asthma. The association of the presence of visible mold and especially mold odor to the risk of asthma points towards mold-related causal agents.

Summaryobjectives Despite a heavy burden of HIV/AIDS and other blood borne infections, few studies have investigated needle stick injuries in sub-Saharan Africa. We conducted a cross-sectional study at Mulago national referral hospital in Kampala, Uganda, to assess the occurrence and risk factors of needle stick injuries among nurses and midwives.methods A total of 526 nurses and midwives involved in the direct day-to-day management of patients answered a questionnaire inquiring about occurrence of needle stick injuries and about potential predictors, including work experience, work load, working habits, training, and risk behaviour.results A 57% of the nurses and midwives had experienced at least one needle stick injury in the last year. Only 18% had not experienced any such injury in their entire career. The rate of needle stick injuries was 4.2 per person-year. Multiple logistic regression analysis showed that the most important risk factor for needle stick injuries was lack of training on such injuries (OR 5.72, 95% CI 3.41-9.62).Other important risk factors included working for more than 40 h/week (OR 1.90, 95% CI 1.20-3.31), recapping needles most of the time (OR 1.78, 95% CI 1.11-2.86), and not using gloves when handling needles (OR 1.91, 95% CI 1.10-3.32).conclusions The study showed a high rate of needle stick injuries among nurses and midwives working in Uganda. The strongest predictor for needle stick injuries was lack of training. Other important risk factors were related to long working hours, working habits, and experience.

BackgroundA substantial number of epidemiologic studies have provided estimates of the relation between exposure to benzene at work and the risk of leukemia, but the results have been heterogeneous. To bridge this gap in knowledge, we synthesized the existing epidemiologic evidence on the relation between occupational exposure to benzene and the risk of leukemia, including all types combined and the four main subgroups acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML).MethodsA systematic literature review was carried out using two databases 'Medline' and 'Embase' from 1950 through to July 2009. We selected articles which provided information that can be used to estimate the relation between benzene exposure and cancer risk (effect size).ResultsIn total 15 studies were identified in the search, providing 16 effect estimates for the main analysis. The summary effect size for any leukemia from the fixed-effects model was 1.40 (95% CI, 1.23-1.57), but the study-specific estimates were strongly heterogeneous (I2 = 56.5%, Q stat = 34.47, p = 0.003). The random-effects model yielded a summary- effect size estimate of 1.72 (95% CI, 1.37-2.17). Effect estimates from 9 studies were based on cumulative exposures. In these studies the risk of leukemia increased with a dose-response pattern with a summary-effect estimate of 1.64 (95% CI, 1.13-2.39) for low (< 40 ppm-years), 1.90 (95% CI, 1.26-2.89) for medium (40-99.9 ppm-years), and 2.62 (95% CI, 1.57-4.39) for high exposure category (> 100 ppm-years). In a meta-regression, the trend was statistically significant (P = 0.015). Use of cumulative exposure eliminated heterogeneity. The risk of AML also increased from low (1.94, 95% CI, 0.95-3.95), medium (2.32, 95% CI, 0.91-5.94) to high exposure category (3.20, 95% CI, 1.09-9.45), but the trend was not statistically significant.ConclusionsOur study provides consistent evidence that exposure to benzene at work increases the risk of leukemia with a dose-response pattern. There was some evidence of an increased risk of AML and CLL. The meta-analysis indicated a lack of association between benzene exposure and the risk of CML.

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