The impact of long-term PM2.5 exposure on specific causes of death: exposure-response curves and effect modification among 53 million U.S. Medicare beneficiaries.

BACKGROUND: The shape of the exposure-response curve for long-term ambient fine particulate (PM2.5) exposure and cause-specific mortality is poorly understood, especially for rural populations and underrepresented minorities. METHODS: We used hybrid machine learning and Cox proportional hazard models to assess the association of long-term PM2.5 exposures on specific causes of death for 53 million U.S. Medicare beneficiaries (aged ≥65) from 2000 to 2008. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES) in our main analyses, with approximately 4 billion person-months of follow-up, and additionally for warm season average of 1-h daily maximum ozone exposures in a sensitivity analysis. The impact of non-traffic PM2.5 on mortality was examined using two stage models of PM2.5 and nitrogen dioxide (NO2). RESULTS: A 10 µg /m3 increase in 12-month average PM2.5 prior to death was associated with a 5% increase in all-cause mortality, as well as an 8.8, 5.6, and 2.5% increase in all cardiovascular disease (CVD)-, all respiratory-, and all cancer deaths, respectively, in age, gender, race, ZIP code, and SES-adjusted models. PM2.5 exposures, however, were not associated with lung cancer mortality. Results were not sensitive to control for ozone exposures. PM2.5-mortality associations for CVD- and respiratory-related causes were positive and significant for beneficiaries irrespective of their sex, race, age, SES and urbanicity, with no evidence of a lower threshold for response or of lower Risk Ratios (RRs) at low PM2.5 levels. Associations between PM2.5 and CVD and respiratory mortality were linear and were higher for younger, Black and urban beneficiaries, but were largely similar by SES. Risks associated with non-traffic PM2.5 were lower than that for all PM2.5 and were null for respiratory and lung cancer-related deaths. CONCLUSIONS: PM2.5 was associated with mortality from CVD, respiratory, and all cancer, but not lung cancer. PM2.5-associated risks of CVD and respiratory mortality were similar across PM2.5 levels, with no evidence of a threshold. Blacks, urban, and younger beneficiaries were most vulnerable to the long-term impacts of PM2.5 on mortality.

Prevalence of loud leisure noise activities among a representative sample of Canadians aged 6-79 years.

This population-based study estimates the prevalence of loud leisure noise exposure and hearing protection usage among Canadians, as well as the population potentially at-risk using an occupational limit of 85 dBA, LEX 40 h, which denotes a typical occupational noise limit for a 40 hour work week. A total of 10 460 participants, aged 6-79 years, completed a Canadian Health Measures Survey household questionnaire. Loud leisure noise was defined by vocal effort required while communicating at arm's length except for loud personal listening device (PLD) usage with earbuds/headphones, which included both volume setting and vocal effort. The most prevalent loud leisure noise activities were amplified music, car/home stereo listening, and power tools, with 40% reporting each source, followed by sporting/entertainment (25%), gasoline engines (23%), and loud PLD listening (19.5%). Loud leisure noise was more prevalent among 12-39 year olds and males. Hearing protection usage was uncommon, from 44.2% (firearms) to 20.3% (power tools) and below 3% during amplified music and sporting/entertainment events. Calculations using self-reported duration of loud leisure noise activities estimated that 6.6 × 106 Canadians were in the high cumulative noise exposure category. A large proportion of Canadians would be expected to develop some degree of noise-induced hearing loss should this pattern persist over years.

[Classification and risk assessment: complementary or mutually exclusive approaches?] / Classificazione delle sostanze e valutazione del rischio chimico: approcci complementari o incompatibili?

OBJECTIVES: Most classification schemes are based on hazard identification: this is particularly true for carcinogenic and reproductive effects. METHODS: These schemes are no longer adequate to take adequate decisions on risk management, and they appear outmoded. In addition, the induce communication and perception problems in the population, causing health scares and anxiety that are difficult to control and recover. RESULTS: Risk assessment requires an estimation of human exposure to be compared with the safe dose for humans (exposure or intake limits) estimated after hazard characterization based on dose-response relationship. CONCLUSIONS: The risk based approaches provide quantitative information on the potency of the substance that can be compared with duration, frequency and intensity of exposure and, therefore, properly inform graded risk management decisions, in relation to the expected characteristics of exposure.

Modeling horizontal and vertical variation in intraurban exposure to PM2.5 concentrations and compositions.

Land use regression (LUR) models are increasingly used to evaluate intraurban variability in population exposure to fine particulate matter (PM2.5). However, most of these models lack information on PM2.5 elemental compositions and vertically distributed samples. The purpose of this study was to evaluate intraurban exposure to PM2.5 concentrations and compositions for populations in an Asian city using LUR models, with special emphasis on examining the effects of having measurements on different building stories. PM2.5 samples were collected at 20 sampling sites below the third story (low-level sites). Additional vertically stratified sampling sites were set up on the fourth to sixth (mid-level sites, n=5) and seventh to ninth (high-level sites, n=5) stories. LUR models were built for PM2.5, copper (Cu), iron (Fe), potassium (K), manganese (Mn), nickel (Ni), sulfur (S), silicon (Si), and zinc (Zn). The explained concentration variance (R(2)) of the PM2.5 model was 65%. R(2) values were >69% in the Cu, Fe, Mn, Ni, Si, and Zn models and <44% in the K and S models. Sampling height from ground level was a significant predictor in the PM2.5 and Si models. This finding stresses the importance of collecting vertically stratified information on PM2.5 mass concentrations to reduce potential exposure misclassification in future health studies. In addition to traffic variables, some models identified gravel-plant, industrial, and port variables with large buffer zones as important predictors, indicating that PM from these sources had significant effects at distant places.

A case-control study of medium-term exposure to ambient nitrogen dioxide pollution and hospitalization for stroke.

BACKGROUND: There are several plausible mechanisms whereby either short or long term exposure to pollution can increase the risk of stroke. Over the last decade, several studies have reported associations between short-term (day-to-day) increases in ambient air pollution and stroke. The findings from a smaller number of studies that have looked at long-term exposure to air pollution and stroke have been mixed. Most of these epidemiological studies have assigned exposure to air pollution based on place of residence, but these assignments are typically based on relatively coarse spatial resolutions. To date, few studies have evaluated medium-term exposures (i.e, exposures over the past season or year). To address this research gap, we evaluated associations between highly spatially resolved estimates of ambient nitrogen dioxide (NO2), a marker of traffic pollution, and emergency department visits for stroke in Edmonton, Canada. METHODS: This was a case-control study with cases defined as those who presented to an Edmonton area hospital emergency department between 2007 and 2009 with an acute ischemic stroke, hemorrhagic stroke, or transient ischemic attack. Controls were patients who presented to the same emergency departments for lacerations, sprains, or strains. A land-use regression model provided estimates of NO2 that were assigned to the place of residence. Logistic regression methods were used to estimate odds ratios for stroke in relation to an increase in the interquartile range of NO2 (5 ppb), adjusted for age, sex, meteorological variables, and neighborhood effects. RESULTS: The study included 4,696 stroke (cases) and 37,723 injury patients (controls). For all strokes combined, there was no association with NO2. Namely, the odds ratio associated with an interquartile increase in NO2 was 1.01 (95% confidence interval {CI}: 0.94-1.08). No associations were evident for any of the stroke subtypes examined. CONCLUSION: When combined with our earlier work in Edmonton, our findings suggest that day-to-day fluctuations in air pollution increase the risk of ischemic stroke during the summer season, while medium term exposures are unrelated to stroke risk. The findings for medium term exposure should be interpreted cautiously due to limited individual-level risk factor data.

Cancer and environment: definitions and misconceptions.

BACKGROUND: Scientific evidence supports an association between environmental exposures and cancer. However, a reliable estimate for the proportion of cancers attributable to environmental factors is currently unavailable. This may be related to the varying definitions of the term "environment." The current review aims to determine how the reporting of the definition of the environment and of the estimates of environmentally attributable risks have changed over the past 50 years. METHODS: A systematic literature search was performed to retrieve all relevant publications relating to the environment and cancer from January 1960 to December 2010 using PubMed, EMBASE, Scopus, and Web of Science. Definitions of the environment and environmentally attributable risks for cancer were extracted from each relevant publication. RESULTS: The search resulted in 261 relevant publications. We found vast discrepancies in the definition of the environment, ranging from broad (including lifestyle factors, occupational exposures, pollutants, and other non-genetic factors) to narrow (including air, water, and soil pollutants). Reported environmentally attributable risk estimates ranged from 1% to 100%. CONCLUSIONS: Our findings emphasize the discrepancies in reporting environmental causation of cancer and the limits of inference in interpreting environmentally attributable risk estimates. Rather than achieving consensus on a single definition for the environment, we suggest the focus be on achieving transparency for any environmentally attributable risks.

Altitude and environmental climate effects on bronchiolitis severity among children presenting to the emergency department.

Bronchiolitis, a respiratory illness, is the leading cause of hospitalization for infants. The authors examined whether environmental factors contributed to the severity of the bronchiolitis illness. They compiled environmental data (temperature, dew point, wind speed, precipitation, altitude, and barometric pressure) to augment clinical data from a 30-center prospective cohort study of emergency department patients with bronchiolitis. They analyzed these data using multivariable logistic regression. Higher altitude was modestly associated with increased retractions (odds ratio [OR] = 1.6; 95% confidence interval [CI] = 1.1-2.1; p < .001) and decreased air entry (OR = 2.0; 95% CI = 1.6-2.6; p < .001). Increasing wind speed had a minor association with more severe retractions (OR = 1.3; 95% CI = 1.1-1.7; p = .02). Higher dew points had a minor association with lower admission rates (OR = 0.9; 95% CI = 0.8-0.996; p = .04). Altitude and environmental climate variables appear to have modest associations with the severity of bronchiolitis in the emergency department. Further studies need to be conducted, however, on limiting exposure to these environmental variables or increasing humidity before making broad recommendations.

Attrition in a panel study of people with environmental exposures: new insights about the impact of race, sex, and number of children in the household.

This study examines attrition in a panel survey. Each member of the panel was selected because of their documented exposure to long-term, low levels of hazardous substances in their residential water. In addition, each was informed of their exposure at the time of baseline contact. The analytic approach involves examining the interactive effect of race and sex, as well as the additive effect of household characteristics on the propensity to stay. The data are derived from the National Exposure Registry, which is a large-scale, longitudinal health survey. This study finds that compared with white males, non-white males are more likely to attrite and white females are more likely to stay in the study. In addition, the propensity to stay is affected by the number of children in the household. These findings have implications for field procedures that may involve the selective targeting at baseline of those subgroups with a greater propensity to attrite.

The psychological impact of terrorist attacks: examining a dose-response relationship between exposure to 9/11 and Axis I mental disorders.

BACKGROUND: Previous research has suggested a dose-response relationship between exposure to the 9/11 terrorist attacks and posttraumatic stress disorder (PTSD) and depression. However, this relationship has not been examined with other Axis I mental disorders. This study examined whether the incidence of Axis I mental disorders was associated with level of exposure to the 9/11 terrorist attacks. METHOD: Data came from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-2; N=34,653, ages 20+) collected between 2004 and 2005. This survey utilized a fully structured face-to-face interview to assess the presence of DSM-IV Axis I disorders since Wave 1 of the NESARC, collected between 2001 and 2002. Multiple logistic regression analyses were employed to examine the relationship between the level of exposure to 9/11 and the prevalence of Axis I disorders since Wave 1. RESULTS: In adjusted models, higher levels of exposure increased the odds of having new onset PTSD, any anxiety disorder, and any mental disorder. Compared to participants who were not exposed to 9/11, those who directly experienced 9/11 had six times the odds of having PTSD, 2.5 times the odds of having any anxiety disorder, and nearly twice the odds of having any mental disorder. CONCLUSIONS: Results suggest that there is a dose-response relationship between level of exposure to the 9/11 attacks and PTSD. Furthermore, higher levels of exposure increase the odds of having any anxiety disorder and any Axis I mental disorder.

Urban air pollution and climate change as environmental risk factors of respiratory allergy: an update.

The incidence of allergic respiratory diseases and bronchial asthma appears to be increasing worldwide, and people living in urban areas more frequently experience these conditions than those living in rural areas. One of the several causes of the rise in morbidity associated with allergic respiratory diseases is the increased presence of outdoor air pollutants resulting from more intense energy consumption and exhaust emissions from cars and other vehicles. Urban air pollution is now a serious public health hazard. Laboratory studies confirm epidemiologic evidence that air pollution adversely affects lung function in asthmatics. Damage to airway mucous membranes and impaired mucociliary clearance caused by air pollution may facilitate access of inhaled allergens to the cells of the immune system, thus promoting sensitization of the airway. Consequently, a more severe immunoglobulin (Ig) E-mediated response to aeroallergens and airway inflammation could account for increasing prevalence of allergic respiratory diseases in polluted urban areas. The most abundant components of urban air pollution in urban areas with high levels of vehicle traffic are airborne particulate matter, nitrogen dioxide, and ozone. In addition, the earth's temperature is increasing, mainly as a result of anthropogenic factors (e.g., fossil fuel combustion and greenhouse gas emissions from energy supply, transport, industry, and agriculture), and climate change alters the concentration and distribution of air pollutants and interferes with the seasonal presence of allergenic pollens in the atmosphere by prolonging these periods.

[Problems and perspectives in the hygienic regulation of biotechnological strains of microorganisms].

The state-of-the-art of hygienic standardization of biotechnological strains of microorganisms is considered. The last century's investigations accumulated abundant experimental data on the estimation of the adverse effect of the strains, formulated main guidelines for evaluating the negative activity of producing strains, and proposed a schematic diagram for toxicological and hygienic investigations of new biotechnological strains. Further studies made it possible to elaborate their human hazard classification, to improve study programs, to substantiate a priority list, and to develop approaches to assessing the occupational microbiological risk.

Variations in Athlete Heat-Loss Potential Between Hot-Dry and Warm-Humid Environments at Equivalent Wet-Bulb Globe Temperature Thresholds.

CONTEXT: Many organizations associated with sports medicine recommend using wet-bulb globe temperature (WBGT)-based activity-modification guidelines that are uniform across the country. However, no consideration has been given to whether the WBGT thresholds are appropriate for different weather conditions, such as warm-humid (WH) relative to hot-dry (HD), based on known differences in physiological responses to these environments. OBJECTIVE: To identify if personnel in regions with drier conditions and greater evaporative cooling potential should consider using WBGT-based activity-modification thresholds that differ from those in more humid weather. DESIGN: Observational study. SETTING: Weather stations across the contiguous United States. MAIN OUTCOME MEASURE(S): A 15-year hourly WBGT dataset from 217 weather stations across the contiguous United States was used to identify particular combinations of globe temperature, wet-bulb temperature, and air temperature that produce WBGTs of 27.9°C, 30.1°C, and 32.3°C. A total of 71 302 observations were clustered into HD and WH environmental conditions. From these clusters, maximum heat-loss potential and heat-flux values were modeled at equivalent WBGT thresholds with various activity levels, clothing, and equipment configurations. RESULTS: We identified strong geographic patterns, with HD conditions predominant in the western half and WH conditions predominant in the eastern half of the country. Heat loss was systematically greater in HD than in WH conditions, indicating an overall less stressful environment, even at equivalent WBGT values. At a WBGT of 32.3°C, this difference was 11 W·m-2 at an activity velocity of 0.3 m·s-1, which doubled for an activity velocity of 0.7 m·s-1. The HD and WH difference increased with the WBGT value, demonstrating that evaporative cooling differences between HD and WH conditions were even greater at a higher, rather than lower, WBGT. CONCLUSIONS: Potential heat loss was consistently greater in HD than in WH environments despite equal WBGTs. These findings support the need for further clinical studies to determine the appropriate WBGT thresholds based on environmental and physiological limits to maximize safety while avoiding unnecessary limitations.

Cardiovascular Risk in COPD: Deciphering the Contribution of Tobacco Smoking.

BACKGROUND: The observation that COPD is an independent risk factor for cardiovascular disease (CVDs) comes from comparisons between smokers with COPD and smokers without COPD. The mechanisms that explain increased risk of CVD in patients with COPD are still unclear. OBJECTIVES: The goal of this study was to assess systemic arterial stiffness (a predictor of CVD mortality) and to evaluate its determinants in a group of patients with mild to moderate COPD secondary to organic dust exposure, tobacco smoking, or both. METHODS: Systemic arterial stiffness was assessed by using aortic pulse wave velocity (aPWV). Measurements were made in 142 patients with COPD and 155 healthy control subjects matched for age, sex, BMI, and tobacco smoking, exposed to tobacco smoking (n = 56/70 for COPD/control subjects, respectively), organic dusts (n = 44/48), or both (n = 42/37). RESULTS: aPWV was higher in COPD than in healthy controls in subjects exposed to tobacco smoking and to both organic dusts and tobacco smoking. By contrast, among never smokers exposed to organic dusts, patients with COPD and matched control subjects had similar aPWV. Multivariate analysis of the 142 patients with COPD (exposed to tobacco smoking and/or to organic dusts) showed that tobacco smoking was associated with high aPWV. Moreover, soluble suppression of tumorigenicity 2, a marker of major cardiovascular events, was correlated with aPWV in these patients. CONCLUSIONS: Analysis of an unselected group of patients with COPD with different causes suggests that: (1) COPD by itself is not sufficient to explain increased aPWV; and (2) tobacco smoking is a risk factor for elevated aPWV in COPD.

Air pollution and risk of stroke: underestimation of effect due to misclassification of time of event onset.

BACKGROUND: Epidemiologic studies linking ambient air pollution to the onset of acute cardiovascular events often rely on date of hospital admission for exposure assessment. METHODS: We investigated the extent of exposure misclassification resulting from assigning exposure to particulate matter based on (1) date of hospital admission, or (2) time of hospital presentation compared with particulate matter exposure based on time of stroke symptom onset. We performed computer simulations to evaluate the impact of this source of exposure misclassification on estimates of air pollution health effects in the context of a time-stratified case-crossover study. RESULTS: Among 1101 patients admitted for a confirmed acute ischemic stroke to a Boston area hospital, symptom onset occurred a median of 1 calendar day before hospital admission (range = 0-30 days). The difference between ambient particulate matter exposure based on the calendar day of admission versus time of symptom onset ranged from -47 to 36 microg/m3 (-0.1 +/- 7.1 microg/m3; mean +/- SD). The simulation study indicated that for nonnull associations, exposure assessment based on hospitalization date led to estimates that were biased toward the null by 60%-66%, whereas assessment based on time of hospital presentation yielded estimates that were biased toward the null by 37%-42%. CONCLUSIONS: Epidemiologic studies of air pollution-related risk of acute cardiovascular events that assess exposure based on date of hospitalization likely underestimate the strength of associations. Using data on time of hospital presentation would marginally attenuate, but not eliminate, this important source of bias.

Chemically induced pheochromocytomas in rats: mechanisms and relevance for human risk assessment.

Pheochromocytomas are tumors originating from chromaffin cells of the adrenal medulla, which have been observed in numerous carcinogenicity studies. The authors have evaluated pheochromocytoma concurrence with other effects and the possible mechanisms, in order to assess the relevance of such data for the classification of carcinogenic effects and their relevance to humans. The evaluation revealed that pheochromocytomas occur with relatively higher frequency in male rats, especially when the following conditions are involved: hypoxia, uncoupling of oxidative phosphorylation, disturbance in calcium homeostasis, and disturbance of the hypothalamic endocrine axis. The underlying biochemical mechanisms suggest that other substances that interfere with these biochemical endpoints also produce pheochromocytomas. Such endpoints include enzymes involved in catecholamine synthesis, receptor tyrosine kinase (RET), hypoxia-inducible factor (HIF), succinate dehydrogenase, fumarate hydratase, and pyruvate dehydrogenase. To date, there is no indication that the substances inducing pheochromocytomas in animal experiments also induce corresponding tumors in humans. Because the mechanisms of action identified in rats are to be expected in humans, pheochromocytomas may be induced after exposure conditions similar to those used in the animal studies. Whether hereditary mutations represent a risk factor in humans is not clear. Pheochromocytomas that occur in animal experiments currently appear to have little relevance for conditions at the work place. When sufficiently documented and evaluated, such secondary pheochromocytomas are not relevant for classification and human risk assessment.

Development of a method for personal, spatiotemporal exposure assessment.

This work describes the development and evaluation of a high resolution, space and time-referenced sampling method for personal exposure assessment to airborne particulate matter (PM). This method integrates continuous measures of personal PM levels with the corresponding location-activity (i.e. work/school, home, transit) of the subject. Monitoring equipment include a small, portable global positioning system (GPS) receiver, a miniature aerosol nephelometer, and an ambient temperature monitor to estimate the location, time, and magnitude of personal exposure to particulate matter air pollution. Precision and accuracy of each component, as well as the integrated method performance were tested in a combination of laboratory and field tests. Spatial data was apportioned into pre-determined location-activity categories (i.e. work/school, home, transit) with a simple, temporospatially-based algorithm. The apportioning algorithm was extremely effective with an overall accuracy of 99.6%. This method allows examination of an individual's estimated exposure through space and time, which may provide new insights into exposure-activity relationships not possible with traditional exposure assessment techniques (i.e., time-integrated, filter-based measurements). Furthermore, the method is applicable to any contaminant or stressor that can be measured on an individual with a direct-reading sensor.

Sources of lead exposure in various countries.

This review evaluates the sources of lead exposure worldwide. Studies from searches relating to sources of lead exposure in various countries within different regional zones were reviewed. Results indicated that in Nigeria, exposure sources include electronic waste, paint and batteries. In Mexico exposure sources include glazed ceramics, lead contaminated utensils and lead contaminated water, for India lead sources include cosmetics and traditional medicines. Sources of lead exposure in China include e-waste, traditional medicines and industrial emissions. In France, exposure sources included lead paint from older homes, imported ceramics and cosmetics and industrial emissions. Australia's exposure sources include paint, dust, imported toys and traditional medicines. Finally, in the United States exposure sources included paint, the industrial legacy of lead exposure and batteries. In high-income countries (HICs) the legacy of lead exposure keeps populations continuously exposed. In lower- and middle-income countries (LMICs), in addition to the legacy of lead exposure, lack of regulations or the inability to enforce regulations keeps populations exposed. In all, evidence suggests that lead exposure remains an issue of public health significance in both HIC and LMIC.

Biomonitoring and Nonpersistent Chemicals-Understanding and Addressing Variability and Exposure Misclassification.

PURPOSE OF REVIEW: We offer here a review of intraindividual variability in urinary biomarkers for assessing exposure to nonpersistent chemicals. We provide thoughts on how to better evaluate exposure to nonpersistent chemicals. RECENT FINDINGS: We summarized reported values of intraclass correlation coefficients and found that most values fall into categories that indicate only poor to good reproducibility. Even within the "good" classification, a large percentage of study participants is likely to be misclassified as to their exposure. There is sufficient information to support the statement that studies using only one spot measurement of a nonpersistent chemical will be unreliable. It is unequivocal that multiple samples have to be collected over a period of toxicological relevance and with consideration of exposure patterns. Sponsors of research and researchers themselves should be vocal about ensuring that sufficient resources are made available to properly characterize exposures when studying nonpersistent chemicals. Otherwise, we will continue to see an ever-growing body of literature yielding inconsistent and/or uninterpretable results.