Suchergebnisse

Radon, a long‐established cause of lung cancer in uranium and other underground miners, has recently emerged as a potentially important cause of lung cancer in the general population. The evidence for widespread exposure of the population to radon and the well‐documented excess of lung cancer among underground miners exposed to radon decay products have raised concern that exposure to radon progeny might also be a cause of lung cancer in the general population. To date, epidemiological data on the lung cancer risk associated with environmental exposure to radon have been limited. Consequently, the lung cancer hazard posed by radon exposure in indoor air has been addressed primarily through risk estimation procedures. The quantitative risks of lung cancer have been estimated using exposure‐response relations derived from the epidemiological investigations of uranium and other underground miners. We review five of the more informative studies of miners and recent risk projection models for excess lung cancer associated with radon. The principal models differ substantially in their underlying assumptions and consequently in the resulting risk projections. The resulting diversity illustrates the substantial uncertainty that remains concerning the most appropriate model of the temporal pattern of radon‐related lung cancer. Animal experiments, further follow‐up of the miner cohorts, and well‐designed epidemiological studies of indoor exposure should reduce this uncertainty.

Demonstration of a dose‐response relationship for environmental tobacco smoke (ETS) is an important indication of causality. Central to the analysis and interpretation of dose‐response relations as described in epidemiological studies is the relationship between dose and exposure. It must be recognized that in studies of ETS we have only surrogate measures of dose, and these surrogate measures (based on exposure) are imperfect. The question‐based measures of ETS exposure generally have not been standardized, may have limited validity and reliability, and cannot comprehensively describe total ETS exposure, exposure to individual ETS components, nor doses of biologically relevant agents at target sites. Nevertheless, useful data have been yielded in epidemiologic studies linking ETS exposure to increased respiratory infection and symptoms, reduced lung growth in children, and increased lung cancer in nonsmoking adults. The more consistent exposure‐response data for studies on acute health in children may reflect the greater difficulty in measuring exposure in studies of chronic health in adults.SUMMARYFor children, adverse effects have been causally associated with exposure to ETS. The epidemiological evidence and the supporting toxicological data link ETS to increased lower respiratory illness, increased respiratory symptoms, and reduced lung growth. Exposure‐response relationships have been described for these effect; errors in exposure estimates would tend to lessen rather than to exaggerate these relationships. By contrast, in adults, the evidence for adverse cardiopulmonary effects of ETS exposures, other than lung cancer, it's presently less conclusive. Misclassification of exposure may be more severe for adults than for children, and the resulting bias toward the null may obscure effects of respiratory symptoms and lung function. Research on adults is hindered by the difficulty of estimating exposures received in diverse environments over a lengthy period. Continued controversy related to the effects of ETS exposure in the workplace and in public locations provides a rationale for further research. However, more valid methods for assessing the exposures of adults to ETS are needed for such research.

The coronavirus disease 2019 (COVID-19) pandemic is an unprecedented challenge for society, affecting those already subject to unacceptable health inequalities and resulting in vast economic impacts. The pandemic reminds everyone of the value and necessity of public health. In the context of an era that will be shaped by COVID-19, we outline the coming series of challenges and transitions in public health and the needed actions over the next 5 years to reinvent our public health systems. Multiple limitations in current US and global public health systems have been uncovered by the pandemic, including insufficient preparedness and surveillance capabilities complicated by long-standing and worsening health inequalities and the rapid spread of misinformation that needs to be countered. We foresee 3 phases for public health over the next 5 years: (1) reactive crisis management, (2) efforts to maintain initial gains, and (3) efforts to sustain and enhance progress. A reinvented public health system will depend highly on leadership and political will, rethinking how we categorize and address population-level risk, employing 21st-century data sciences, and applying new communication skills.