Objective: This study aimed to assess whether screen time differs across combined migration-obesity and migration-smoking profiles among Mexican-born non-migrants living in Mexico, Mexican-born immigrants residing in the United States, and U.S.-born individuals of Mexican origin. Material and Methods: We conducted a cross-sectional comparison using two national databases. Multinomial regression models were used to assess differences in screen time across combined migration-obesity and migration-smoking profiles. The study population was classified into three groups: U.S.-born individuals of Mexican origin, Mexican-born migrants residing in the United States, and Mexican-born non-migrants residing in Mexico. Results: Migration status was significantly associated with screen time, with significant associations involving smoking and obesity. In adjusted analyses, U.S.-born individuals of Mexican origin who reported tobacco use or obesity had the highest Adjusted Relative Risk Ratio (ARRR) for spending more than 4 hours per day on screen time compared to the reference < 2 hours per day. Mexican immigrants in the U.S. Additionally, Mexican immigrants in the U.S. showed increased risks of obesity and smoking, along with higher screen time (> 4 vs. < 2hours/day), compared to non-migrants residing in Mexico. Conclusions: This cross-sectional binational study highlights that migrant populations exhibit higher screen time combined with risk factors such as obesity and smoking. This profile reflects a risky pattern for Mexican populations migrating to the U.S., highlighting the need for binational public health strategies that address lifestyle impacts in the migration process. Keywords: Sedentary behavior; Smoking; Obesity; Migration.
The Nuclear Age spurred widespread mining of uranium for production of weapons and for nuclear power. The widespread mining of uranium, with historically limited control of radiation exposures, has resulted in high rates of lung cancer among the former miners. This paper reviews the long and ongoing story of lung cancer among miners of uranium.
Globally, in 2019, chronic obstructive pulmonary disease (COPD) was the third leading cause of death. While tobacco smoking is the predominant risk factor, the role of long-term air pollution exposure in increasing risk of COPD remains unclear. Moreover, there are few studies that have been conducted in racial and ethnic minoritized and socioeconomically diverse populations, while accounting for smoking history and other known risk factors. To evaluate the association for ambient air pollution and COPD in a multiethnic population in California. Among 38,654 African American, Japanese American, Latino and White California participants in the Multiethnic Cohort study enrolled in the fee-for-service component of Medicare, we used Cox proportional hazards regression to estimate the association of time-varying ambient air pollutants: particulate matter with diameter ≤2.5 μm or 10 μm (PM2.5, PM10), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), benzene and ultrafine particles (UFP) with COPD risk (n=10,915 cases; 8.8 years of follow-up). Subgroup analyses were conducted by race and ethnicity, sex, smoking status at MEC baseline questionnaire, and neighborhood socioeconomic status (nSES). We observed positive associations for NOx (per 50 ppb) with risk of COPD (hazards ratios (HR)=1.45; 95% CI: 1.35-1.55). The associations for NO2 (per 20 ppb), PM2.5 (10ug/m3), PM10 (10ug/m3), CO (1000 ppb), and UFP (IQR=5241.7 particles/cm3) with risk of COPD were in similar directions as these air pollutants are highly correlated with NOx. These associations were found in African American, Latino, and Japanese American participants, but not in whites (p-heterogeneity across race and ethnicity<0.04). These associations also differed by nSES with effects being stronger in racial and ethnic minoritized populations and residents of low SES neighborhoods. Long-term ambient air pollutant exposure is associated with COPD risk in a multiethnic, older adult (>65 years of age), population.
Progressive legalization of medical and recreational cannabis markets at the state-level has led to rapid growth of medical and recreational cannabis markets and to product diversification with emerging products having high concentrations of delta-9-tetrahydrocannabinol. Research on these products is still limited and the evidence available for policy formulation is diminished by methodological limitations. As a step towards addressing these limitations, the Colorado School of Public Health convened a multidisciplinary workshop that addressed four areas of cannabis research: epidemiological, clinical, surveillance, and policy. Workshop participants provided recommendations in each area to advance research on cannabis to make it more informative for decision-making on key policy topics. Emphasis was placed on assessment of use of cannabis products by study participants. Recommendations for research methods and their implementation were made in the four areas. Those for epidemiology include using a core set of exposure assessment measures across three domains; developing this core set through a national and/or international scientific consensus process; ensuring the core set of measures are validated and readily available; and updating the core set periodically to account for ongoing changes in the cannabis landscape. Recommendations in the clinical research area include standard dosing and dosing terminology; standardized data collection instruments; identifying biomarkers for detecting cannabis exposure; and biological matrices. Policy research recommendations were offered for state regulators, evaluators/researchers, and policy makers. Surveillance recommendations include developing and implementing a novel and nimble surveillance system to monitor use of high-concentration forms of cannabis; adding questions to existing surveillance systems with the objective of monitoring high-concentration cannabis and adverse outcomes; and elevating the coordination, synthesis, and dissemination of findings in existing data sources that could signal adverse outcomes from high-concentration cannabis. Given the changing marketplace, it is urgent to improve the informativeness of cannabis research through enhanced research methods.
The year 2025 marks the 80th anniversary of one of the worst human-caused tragedies: the atomic bombings of Hiroshima and Nagasaki, with acute death tolls of approximately 140,000 in Hiroshima and 74,000 in Nagasaki by the end of 1945. This editorial provides historical and social context for the articles in this special issue of Carcinogenesis.
In conducting a scoping review on the health effects of high-concentration cannabis products, we have uncovered pervasive methodological shortcomings within the cannabis literature. This review begins by defining the "causal effect" of interest for public health and delineating the desirable features of study design that can address crucial questions pertaining to public health and policy. We further delve into the methodological complexities inherent in studying the health effects of high-concentration cannabis products, describing challenges associated with the measurement of exposures and outcomes, confounding, selection bias, and the generalizability of findings. We introduce causal inference methods to mitigate potential biases in observational cannabis use studies. We identify specific areas that necessitate further development and investigation to deepen our understanding of this topic. Finally, this review extends actionable recommendations, serving as a roadmap for upcoming research initiatives in this domain.
Rationale: Globally, chronic obstructive pulmonary disease (COPD) was the third leading cause of death in 2019. Although tobacco smoking is the predominant risk factor, the role of long-term air pollution exposure in increasing the risk of COPD remains unclear. Moreover, few studies that account for smoking history and other known risk factors have been conducted in racially and ethnically minoritized and socioeconomically diverse populations. Objectives: We sought to evaluate the association of ambient air pollution with COPD in a multiethnic population in California. Methods: In the Multiethnic Cohort Study of 38,654 African-American, Japanese-American, Latino, and White California participants who were enrolled in the fee-for-service component of Medicare, we used Cox proportional hazards regression to estimate the association of time-varying ambient air pollutants-particulate matter with an aerodynamic diameter ⩽2.5 μm or ⩽10 μm, nitrogen dioxide, carbon monoxide, ozone, benzene, and ultrafine particles (UFPs)-with COPD risk (n = 10,915 cases; 8.8 yr of follow up). Subgroup analyses were conducted by race and ethnicity, sex, smoking status as recorded on the Multiethnic Cohort Study baseline questionnaire, and neighborhood socioeconomic status. Results: We observed a positive association of nitrogen oxide (per 50 ppb) with risk of COPD (hazard ratio = 1.45; 95% confidence interval = 1.35-1.55). The associations of nitrogen dioxide (per 20 ppb), particulate matter with an aerodynamic diameter ⩽2.5 μm (10 μg/m3) or ⩽10 μm (10 μg/m3), carbon monoxide (1,000 ppb), and UFPs (interquartile range = 5,241.7 particles/cm3) with risk of COPD were in similar directions, as these air pollutants are highly correlated with nitrogen oxide. These associations were found in African-American, Latino, and Japanese-American participants, but not in Whites (P heterogeneity across race and ethnicity <0.04). These associations also differed by neighborhood socioeconomic status, with effects being stronger in racially and ethnically minoritized populations and residents of low-SES neighborhoods. Conclusions: Long-term ambient air pollutant exposure is associated with COPD risk in a multiethnic, older adult (age >65 yr) population.
RATIONALE:Electronic cigarette (e-cigarette) aerosol contains volatile aldehydes, including flavourings and oxidant metals with known pulmonary toxicity. OBJECTIVES:To evaluate the associations of e-cigarette use with symptoms of wheeze, bronchitic symptoms and shortness of breath (SOB) across 4 years of prospective data. METHODS:Participants completed questionnaires on respiratory symptoms and past 30-day e-cigarette, cigarette and cannabis use in 2014 (wave 1; N=2094; mean age 17.3 years, SD=0.6 years). Follow-up information was collected in 2015 (wave 2; n=1609), 2017 (wave 3; n=1502) and 2018 (wave 4; n=1637) using online surveys. Mixed-effects logistic regression models evaluated associations of e-cigarette use with respiratory symptoms. MEASUREMENTS AND MAIN RESULTS:Participants were mostly Hispanic white (51.8%) and evenly representative by sex (49.6% female; 50.4% male). Compared with never e-cigarette users, past 30-day e-cigarette users reported increased odds of wheeze (OR 1.81; 95% CI 1.28, 2.56), bronchitic symptoms (OR 2.06; 95% CI 1.58, 2.69) and SOB (OR 1.78; 95% CI 1.23, 2.57), adjusting for study wave, age, sex, race, lifetime asthma diagnosis and parental education. Effect estimates were attenuated (wheeze (OR 1.41; 95% CI 0.99, 2.01), bronchitic symptoms (OR 1.55; 95% CI 1.18, 2.05), SOB (OR 1.48; 95% CI 1.01, 2.18)), after adjusting additionally for current cigarette use, cannabis use and secondhand exposure to e-cigarettes/cigarettes/cannabis. CONCLUSIONS:E-cigarette use in young adults was associated with respiratory symptoms, independent of combustible cannabis and cigarette exposures.
Background The acute health effects of short-term (hours to days) exposure to fine particulate matter (PM2.5) have been well documented; however, the global mortality burden attributable to this exposure has not been estimated. We aimed to estimate the global, regional, and urban mortality burden associated with short-term exposure to PPM2.5 and the spatiotemporal variations in this burden from 2000 to 2019. Methods We combined estimated global daily PM2.5 concentrations, annual population counts, country-level mortality rates, and epidemiologically derived exposure-response functions to estimate the mortality attributable to short-term PM2.5 exposure from 2000 to 2019, in the continental regions and in 13 189 urban centres worldwide at a spatial resolution of 0.1 degrees x 0.1 degrees. We tested the robustness of our mortality estimates with different theoretical minimum risk exposure levels, lag effects, and exposure-response functions. Findings Approximately 1 million (95% CI 690 000-1.3 million) premature deaths per year from 2000 to 2019 were attributable to short-term PM2.5 exposure, representing 2.08% (1.41-2.75) of total global deaths or 17 (11-22) premature deaths per 100 000 population. Annually, 0.23 million (0.15 million-0.30 million) deaths attributable to short-term PM2.5 exposure were in urban areas, constituting 22.74% of the total global deaths attributable to this cause and accounting for 2.30% (1.56-3.05) of total global deaths in urban areas. The sensitivity analyses showed that our worldwide estimates of mortality attributed to short-term PM2.5 exposure were robust. Interpretation Short-term exposure to PM2.5 contributes a substantial global mortality burden, particularly in Asia and Africa, as well as in global urban areas. Our results highlight the importance of mitigation strategies to reduce short-term exposure to air pollution and its adverse effects on human health. Copyright (c) 2024 The Author(s). Published by Elsevier Ltd.
Supplementary Table 3 shows an analysis of the association between Airport-Related UFP and Lung Cancer Risk by Smoking Status and Histology among California MEC Participants between 1993-2013.
Supplementary Table 1 shows an overview of the study characteristics of California Multiethnic Cohort (MEC) Participants at Baseline by Race and Ethnicity between 1993-1996.
Supplementary Table 5 shows an analysis of the association between Airport-Related UFP and Lung Cancer Risk Overall by Histology and Time Period among California MEC participants between 1993-2013.
The COVID-19 pandemic and other ongoing public health challenges have highlighted deficiencies in the US public health system. The United States is in a unique moment that calls for a transformation that builds on Public Health 3.0 and its focus on social determinants of health and partnerships with diverse sectors while also acknowledging how the pandemic altered the landscape for public health. Based on relevant literature, our experience, and interviews with public health leaders, we describe seven areas of focus within three broad categories to support transformational change. Contextual areas of focus include increasing accountability and addressing politicization and polarization. Topical areas of focus highlight prioritizing climate change and sharpening the focus on equity. Technical areas of focus include advancing data sciences, building the workforce, and enhancing communication capacity. A transformed public health system will depend highly on leadership, funding incentives, and both bottom-up and top-down approaches. A broad effort is needed by public health agencies, governments, and academia to accelerate the transition to a next phase for public health.
Supplementary Table 2 shows an analysis of the association between Airport-Related UFP and Squamous Cell Carcinoma Risk by Smoking Status among California MEC participants between 1993-2013.