Integrating research, surveillance, and practice in environmental public health tracking.

The Centers for Disease Control and Prevention in the U.S. Department of Health and Human Services is working with selected state and local health departments, academic centers, and others to develop an environmental public health tracking initiative to improve geographic and temporal surveillance of environmental hazards, exposures, and related health outcomes. The objective is to support policy strategies and interventions for disease prevention by communities and environmental health agencies at the federal, state, and local levels. The first 3 years of the initiative focused on supporting states and cities in developing capacity, information technology infrastructure, and pilot projects to demonstrate electronic linkage of environmental hazard or exposure data and disease data. The next phase requires implementation across states. This transition could provide opportunities to further integrate research, surveillance, and practice through attention to four areas. The first is to develop a shared and transparent knowledge base that draws on environmental health research and substantiates decisions about what to track and the interpretation of results. The second is to identify and address information needs of policy and stakeholder audiences in environmental health. The third is to adopt mechanisms for coordination, decision making, and governance that can incorporate and support the major entities involved. The fourth is to promote disease prevention by systematically identifying and addressing population-level environmental determinants of health and disease

Occupational asthma: a review.

Occupational asthma is the most common form of occupational lung disease in the developed world at the present time. In this review, the epidemiology, pathogenesis/mechanisms, clinical presentations, management, and prevention of occupational asthma are discussed. The population attributable risk of asthma due to occupational exposures is considerable. Current understanding of the mechanisms by which many agents cause occupational asthma is limited, especially for low-molecular-weight sensitizers and irritants. The diagnosis of occupational asthma is generally established on the basis of a suggestive history of a temporal association between exposure and the onset of symptoms and objective evidence that these symptoms are related to airflow limitation. Early diagnosis, elimination of exposure to the responsible agent, and early use of inhaled steroids may play important roles in the prevention of long-term persistence of asthma. Persistent occupational asthma is often associated with substantial disability and consequent impacts on income and quality of life. Prevention of new cases is the best approach to reducing the burden of asthma attributable to occupational exposures. Future research needs are identified

The influence of sex, allergic rhinitis, and test system on nasal sensitivity to airborne irritants: a pilot study.

"Nasal irritant sensitivity" is an important construct in environmental health science; functional measures, however, lack standardization. We performed duplicate measures of nasal irritant perceptual acuity on 16 subjects (evenly divided by sex and seasonal allergy status) using two different test compounds: carbon dioxide (CO2) (detection) and n-propanol (localization). The a priori hypotheses included a) allergic rhinitics will display lower perceptual thresholds than nonrhinitics; b) females will display lower perceptual thresholds than males; and c) estimates of perceptual acuity using the two test systems will be positively correlated. We obtained CO2 detection thresholds using an ascending concentration series, presenting 3-sec pulses of CO2, paired with air in random order, by nasal cannula. We obtained localization thresholds by simultaneously presenting stimuli (ascending concentrations of n-propanol vapor in air) and blanks (saturated water vapor in air) to opposite nostrils, with laterality randomized. In terms of test-retest reliability, individual replicate measures for CO2 detection thresholds correlated more closely than did the localization thresholds of volatile organic compounds (VOC) (r = 0.65 and r = 0.60, respectively). As an intertest comparison, log-transformed individual mean CO2 and VOC measures were positively correlated with an r of 0.63 (p < 0.01). In univariate analyses, sex predicted both log-transformed CO2 and VOC thresholds (females being more "sensitive"; p < 0.05 and 0.001, respectively). Nasal allergies predicted sensory testing results only in the multivariate analysis, and then only for VOC localization (p < 0.05). The question of population variation in nasal irritant sensitivity (as well as the generalizability of results across test compounds) deserves further attention

Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES).

The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p&lt;0.01. There were no effects of ozone on the three primary markers of systemic inflammation and a prothrombotic state: C-reactive protein, monocyte-platelet conjugates, and microparticle-associated tissue factor activity. However, among the secondary endpoints, endothelin-1, a potent vasoconstrictor, increased from pre- to post-exposure with ozone concentration (120 vs 0 ppb: 0.07 pg/mL, 95% confidence interval [CI] 0.01, 0.14; 70 vs 0 ppb: -0.03 pg/mL, CI -0.09, 0.04; p = 0.008). Nitrotyrosine, a marker of oxidative and nitrosative stress, decreased with increasing ozone concentrations, with marginal significance (120 vs 0 ppb: -41.5, CI -70.1, -12.8; 70 vs 0 ppb: -14.2, CI -42.7, 14.2; p = 0.017). GSTM1 status did not modify the effect of ozone exposure on any of the outcomes. These findings from healthy older adults fail to identify any mechanistic basis for the epidemiologically described cardiovascular effects of exposure to ozone. The findings, however, may not be applicable to adults with cardiovascular disease

Associations between historical residential redlining and current age-adjusted rates of emergency department visits due to asthma across eight cities in California: an ecological study.

BackgroundAsthma disproportionately affects communities of colour in the USA, but the underlying factors for this remain poorly understood. In this study, we assess the role of historical redlining as outlined in security maps created by the Home Owners' Loan Corporation (HOLC), the discriminatory practice of categorising neighbourhoods on the basis of perceived mortgage investment risk, on the burden of asthma in these neighbourhoods.MethodsWe did an ecological study of HOLC risk grades and asthma exacerbations in California using the security maps available for the following eight cities: Fresno, Los Angeles, Oakland, Sacramento, San Diego, San Jose, San Francisco, and Stockton. Each census tract was categorised into one of four risk levels (A, B, C, or D) on the basis of the location of population-weighted centroids on security maps, with the worst risk level (D) indicating historical redlining. We obtained census tract-level rates of emergency department visits due to asthma from CalEnviroScreen 3.0. We assessed the relationship between risk grade and log-transformed asthma visit rates between 2011 and 2013 using ordinary least squares regression. We included potential confounding variables from the 2010 Census and CalEnviroScreen 3.0: diesel exhaust particle emissions, PM2·5, and percent of the population living below 2 times the federal poverty level. We also built random intercept and slope models to assess city-level variation in the relationship between redlining and asthma.FindingsIn the 1431 census tracts assessed (64 [4·5%] grade A, 241 [16·8%] grade B, 719 [50·2%] grade C, and 407 [28·4%] grade D), the proportion of the population that was non-Hispanic black and Hispanic, the percentage of the population living in poverty, and diesel exhaust particle emissions all significantly increased as security map risk grade worsened (p&lt;0·0001). The median age-adjusted rates of emergency department visits due to asthma were 2·4 times higher in census tracts that were previously redlined (median 63·5 [IQR 34·3] visits per 10 000 residents per year [2011-13]) than in tracts at the lowest risk level (26·5 [18·4]). In adjusted models, redlined census tracts were associated with a relative risk of 1·39 (95% CI 1·21-1·57) in rates of emergency department visits due to asthma compared with that of lowest-risk census tracts.InterpretationHistorically redlined census tracts have significantly higher rates of emergency department visits due to asthma, suggesting that this discriminatory practice might be contributing to racial and ethnic asthma health disparities.FundingNational Heart Lung Blood Institute

Validation of the Human Ozone Challenge Model as a Tool for Assessing Anti-Inflammatory Drugs in Early Development

This study aimed to test the utility of the ozone challenge model for profiling novel compounds designed to reduce airway inflammation. The authors used a randomized, doubledummy, double-blind, placebo-controlled 3-period crossover design alternating single orally inhaled doses of fluticasone propionate (inhaled corticosteroids, 2mg), oral prednisolone (oral corticosteroids, 50mg), ormatched placebo. At a 2-week interval, 18 healthy ozone responders (>10% increase in sputum neutrophils) underwent a 3-hour ozone (250 ppb)/intermittent exercise challenge starting 1 hour after drug treatment. Airway inflammation was assessed at 2 hours (breath condensate) and 3 hours (induced sputum) after ozone challenge. Compared to placebo, pretreatment with inhaled corticosteroids or oral corticosteroids resulted in a significant reduction (mean [95% confidence interval]) of sputum neutrophils by 62% (35%, 77%) and 64% (39%, 79%) and of sputum supernatant myeloperoxidase by 55% (41%, 66%) and 42% (25%, 56%), respectively. The authors conclude that an optimized ozone challenge model (including ozone responders and ensuring adequate drug levels during exposure) may be useful for testing novel anti-inflammatory compounds in early development

A new potassium-based intermediate and its role in the desorption properties of the K–Mg–N–H system

In situSR-PXD experiments revealed a new reaction mechanism of amide–hydride anionic exchange for the K–Mg–N–H system