Occupational carcinogens are an important cause of death and disability worldwide.

There are a number of measures that quantify the public health burden due to specific risk factors for specific diseases. Although these measures are of importance for policymakers, epidemiologists do not often calculate them or may be unfamiliar with some of the issues involved when they do. The primary measure of interest is the attributable fraction (AF), representing the fraction of cases or deaths from a specific disease that would not have occurred in the absence of exposure to a specific risk factor either in the exposed population or the population as a whole. AFs can be multiplied by the total number of cases of a given disease to obtain a "body count"--the absolute number of preventable cases due to a specific risk factor. Two other measures of public health burden, used in conjunction with AFs, are attributable years-of-life-lost and attributable disability-adjusted life-years. We provide an overview of the AF and related measures and discuss some of the specific issues involved in calculating AFs. These issues include calculating the variance of AFs (such as Monte Carlo sensitivity methods), biases arising from some formulas for the AF, sources of data for calculating AFs, dependence of AFs on basic decisions about what exposure-disease associations are causal, and extrapolation from the source population to the target population.

Background Several studies have shown higher Alzheimer’s disease (AD) incidence rates are in African-Americans (AAs) than Caucasians (CCs). If this finding is consistent across studies, it raises important etiologic questions regarding factors responsible for this discrepancy. It also affects the likely public health burden of AD in the US in the future, as the non-Caucasian population becomes the majority. Objective Estimate the AA/CC rate ratio for AD incidence across all available studies. Methods We conducted a meta-analysis of population-based studies for the rate ratio (RR) of AD incidence for AAs versus CCs, after identifying six relevant studies from the literature. We calculated an AA/CC rate ratio across all studies using inverse-variance weighting, and assessed inter-study heterogeneity. Using these incidence data, as well as data on survival after diagnosis, and on all-cause mortality, we also estimated the US prevalence of AD among AAs and CCs. Results There were six population-based studies with data comparing AD incidence between AAs and CCs, with an estimated 370 AA and 640 CC incident cases. The meta-analysis RR showed that the AD rate for AAs was 64% higher than for CCs (RR = 1.64 (95% CI 1.35–2.00)), with no evidence of heterogeneity. We estimated the current US AD prevalence for ages 65–90 to be 5.5% for CCs, and 8.6% for AAs (prevalence ratio 1.56). Conclusion AAs have an increased risk of incident and prevalent AD compared to CCs for reasons which are unknown, but are hypothesized to reflect biological, psychological, and socioeconomic factors.

Conventional confidence intervals reflect uncertainty due to random error but omit uncertainty due to biases, such as confounding, selection bias, and measurement error. Such uncertainty can be quantified, especially if the investigator has some idea of the amount of such bias. A traditional sensitivity analysis produces one or more point estimates for the exposure effect hypothetically adjusted for bias, but it does not provide a range of effect measures given the likely range of bias. Here the authors used Monte Carlo sensitivity analysis and Bayesian bias analysis to provide such a range, using data from a US silica-lung cancer study in which results were potentially confounded by smoking. After positing a distribution for the smoking habits of workers and referents, a distribution of rate ratios for the effect of smoking on lung cancer, and a model for the bias parameter, the authors derived a distribution for the silica-lung cancer rate ratios hypothetically adjusted for smoking. The original standardized mortality ratio for the silica-lung cancer relation was 1.60 (95% confidence interval: 1.31, 1.93). Monte Carlo sensitivity analysis, adjusting for possible confounding by smoking, led to an adjusted standardized mortality ratio of 1.43 (95% Monte Carlo limits: 1.15, 1.78). Bayesian results were similar (95% posterior limits: 1.13, 1.84). The authors believe that these types of analyses, which make explicit and quantify sources of uncertainty, should be more widely adopted by epidemiologists.

Many studies have investigated the neurodevelopmental effects of prenatal and early childhood exposures to organophosphate (OP) pesticides among children, but they have not been collectively evaluated. The aim of the present article is to synthesize reported evidence over the last decade on OP exposure and neurodevelopmental effects in children. The Data Sources were PubMed, Web of Science, EBSCO, SciVerse Scopus, SpringerLink, SciELO and DOAJ. The eligibility criteria considered were studies assessing exposure to OP pesticides and neurodevelopmental effects in children from birth to 18 years of age, published between 2002 and 2012 in English or Spanish. Twenty-seven articles met the eligibility criteria. Studies were rated for evidential consideration as high, intermediate, or low based upon the study design, number of participants, exposure measurement, and neurodevelopmental measures. All but one of the 27 studies evaluated showed some negative effects of pesticides on neurobehavioral development. A positive dose–response relationship between OP exposure and neurodevelopmental outcomes was found in all but one of the 12 studies that assessed dose–response. In the ten longitudinal studies that assessed prenatal exposure to OPs, cognitive deficits (related to working memory) were found in children at age 7 years, behavioral deficits (related to attention) seen mainly in toddlers, and motor deficits (abnormal reflexes) seen mainly in neonates. No meta-analysis was possible due to different measurements of exposure assessment and outcomes. Eleven studies (all longitudinal) were rated high, 14 studies were rated intermediate, and two studies were rated low. Evidence of neurological deficits associated with exposure to OP pesticides in children is growing. The studies reviewed collectively support the hypothesis that exposure to OP pesticides induces neurotoxic effects. Further research is needed to understand effects associated with exposure in critical windows of development.