Objective This study examined the correlation between manganese exposure and manganese concentrations in different biomarkers. Methods Air measurement data and work histories were used to determine manganese exposure over a workshift and cumulative exposure. Toenail samples (n=49), as well as blood and urine before (n=27) and after (urine, n=26; blood, n=24) a workshift were collected. Results Toenail manganese, adjusted for age and dietary manganese, was significantly correlated with cumulative exposure in months 7-9, 10-12, and 7-12 before toenail clipping date, but not months 1-6. Manganese exposure over a work shift was not correlated with changes in blood nor urine manganese. Conclusions Toenails appeared to be a valid measure of cumulative manganese exposure 7 to 12 months earlier. Neither change in blood nor urine manganese appeared to be suitable indicators of exposure over a typical workshift.

Background: To better understand the mechanism(s) of particulate matter (PM) associated cardiovascular effects, research priorities include identifying the responsible PM characteristics. Evidence suggests that metals play a role in the cardiotoxicity of fine PM (PM 2.5 ) and in exposure-related decreases in heart rate variability (HRV). We examined the association between daytime exposure to the metal content of PM 2.5 and night HRV in a panel study of boilermaker construction workers exposed to metalrich welding fumes.

The effects of work and the conditions of employment on health behaviors and intermediate health conditions have been demonstrated, to the extent that these relationships should be addressed in efforts to prevent chronic disease. However, conventional health promotion practice generally focuses on personal risk factors and individual behavior change. In an effort to find solutions to the myriad of health challenges faced by the American workforce, the U.S. National Institute for Occupational Safety and Health (NIOSH) established the Total Worker Health® (TWH) program. Originally organized around the paradigm of integrating traditional occupational safety and health protections with workplace health promotion, TWH has evolved to a broader emphasis on workplace programs for enhancing worker safety, health, and well-being. Among the research programs and approaches developed by investigators at NIOSH Centers of Excellence for TWH and elsewhere, definitions of ‘integration’ in workplace interventions vary widely. There is no consensus about which organizational or individual outcomes are the most salient, how much to emphasize organizational contexts of work, or which program elements are necessary in order to qualify as ‘Total Worker Health’. Agreement about the dimensions of integration would facilitate comparison of programs and interventions which are self-defined as TWH, although diverse in content. The specific criteria needed to define integration should be unique to that concept—i.e. distinct from and additive to conventional criteria for predicting or evaluating the success of a workplace health program. We propose a set of four TWH-specific metrics for integrated interventions that address both program content and process: (i) coordination and interaction of workplace programs across domains; (ii) assessment of both work and non-work exposures; (iii) emphasis on interventions to make the workplace more health-promoting; and (iv) participatory engagement of workers in pivotal ways during intervention prioritization and planning to develop self-efficacy in addressing root causes, skill transfer, building program ownership, empowerment, and continuous improvement. Thus we find that integration requires organizational change, both to engage two managerial functions with different goals, legal responsibilities, and (often) internal incentives & resources, and also to orient the organization toward salutogenesis. Examples from research activity within the Center for the Promotion of Health in the New England Workplace illustrate how these criteria have been applied in practice.

BackgroundIncreasing evidence suggests that obesity may impart greater susceptibility to adverse effects of air pollution. Particulate matter, especially PM2.5 (particulate matter with aero-dynamic diameter ≤2.5 μm), is associated with increased cardiac events and reduction of heart rate variability (HRV).ObjectivesOur goal was to investigate whether particle-mediated autonomic modulation is aggravated in obese individuals.MethodsWe examined PM2.5-mediated acute effects on HRV and heart rate (HR) using 10 24-hr and 13 48-hr ambulatory electrocardiogram recordings collected from 18 boilermakers (39.5 ± 9.1 years of age) exposed to high levels of metal particulates. Average HR and 5-min HRV [SDNN: standard deviation of normal-to-normal intervals (NN); rMSSD: square-root of mean squared-differences of successive NN intervals; HF: high-frequency power 0.15–0.4 Hz] and personal PM2.5 exposures were continuously monitored. Subjects with body mass index ≥ 30 kg/m2 were classified as obese. Mixed-effect models were used for statistical analyses.ResultsHalf (50%) of the study subjects were obese. After adjustment for confounders, each 1-mg/m3 increase in 4-hr moving average PM2.5 was associated with HR increase of 5.9 bpm [95% confidence interval (CI), 4.2 to 7.7] and with 5-min HRV reduction by 6.5% (95% CI, 1.9 to 11.3%) for SDNN, 1.7% (95% CI, –4.9 to 8.4%) for rMSSD, and 8.8% (95% CI, –3.8 to 21.3%) for HF. Obese individuals had greater PM2.5-mediated HRV reductions (2- to 3-fold differences) than nonobese individuals, and had more PM2.5-mediated HR increases (9-bpm vs. 4-bpm increase in HR for each 1-mg/m3 increase in PM2.5; p < 0.001).ConclusionsOur study revealed greater autonomic cardiac responses to metal particulates in obese workers, supporting the hypothesis that obesity may impart greater susceptibility to acute cardiovascular effects of fine particles.

Background While previous epidemiological studies report adverse effects of long-term noise exposure on cardiovascular health, the mechanisms responsible for these effects are unclear. We sought to elucidate the cardiovascular and stress response to short-term, low (31.5-125 Hz) and high (500 – 2000 Hz) frequency noise exposures. Methods Healthy male (n = 10) participants were monitored on multiple visits during no noise, low- or high-frequency noise exposure scenarios lasting 40 minutes. Participants were fitted with an ambulatory electrocardiogram (ECG) and blood pressure measures and saliva samples were taken before, during and after noise exposures. ECGs were processed for measures of heart rate variability (HRV): high-frequency power (HF), low-frequency power (LF), the root of the mean squared difference between adjacent normal heart beats (N-N) intervals (RMSSD), and the standard deviation of N-N intervals (SDNN). Systolic blood pressure (SBP), diastolic blood pressure (DPB), and pulse were reported and saliva was analyzed for salivary cortisol and amylase. Multivariate mixed-effects linear regression models adjusted for age were used to identify statistically significant difference in outcomes by no noise, during noise or after noise exposure periods and whether this differed by noise frequency. Results A total of 658, 205, and 122, HRV, saliva,and blood pressure measurements were performed over 41 person days. Reductions in HRV (LF and RMSSD) were observed during noise exposure (a reduction of 19%(−35,−3.5) and 9.1%(−17,−1.1), respectively). After adjusting for noise frequency, during low frequency noise exposure, HF, LF, and SDNN were reduced (a reduction of 32%(−57,−6.2), 34%(−52,−15), and 16%(−26,−6.1), respectively and during high frequency noise exposure, a 21%(−39,−2.3) reduction in LF, as compared to during no noise exposure was found. No significant (p>0.05) changes in blood pressure,salivary cortisol or amylase were observed. Conclusions These results suggest that exposure to noise, and in particular, to low-frequency noise negatively impacts HRV. The frequencies of noise should be considered when evaluating the cardiovascular health impacts of exposure.