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.

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.

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.

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.

Early-Life Environmental Exposures and Blood Pressure in Children.

BACKGROUND: Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously. OBJECTIVES: This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children. METHODS: Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously. RESULTS: Decreases in systolic BP were observed with facility density (ß change for an interquartile-range increase in exposure: -1.7 mm Hg [95% confidence interval (CI): -2.5 to -0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (-1.4 mm Hg [95% CI: -2.6 to -0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: -1.6 mm Hg [95% CI: -2.4 to -0.7 mm Hg]), hexachlorobenzene (-1.5 mm Hg [95% CI: -2.4 to -0.6 mm Hg]), and mono-benzyl phthalate (-0.7 mm Hg [95% CI: -1.3 to -0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (-1.4 mm Hg [95% CI: -2.3 to -0.5 mm Hg]) and child DDE concentrations (-1.1 mm Hg [95% CI: -1.9 to -0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: -0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg]). CONCLUSIONS: This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children.

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.

Exposure to environmental toxicants and young children's cognitive and social development.

Background Understanding the role of environmental toxicant exposure on children's development is an important area of inquiry in order to better understand contextual factors that shape development and ultimately school readiness among young children. There is evidence suggesting negative links between exposure to environmental toxicants and negative physical health outcomes (i.e. asthma, allergies) in children. However, research on children's exposure to environmental toxicants and other developmental outcomes (cognitive, socioemotional) is limited. Objectives The goal of the current review was to assess the existing literature on the links between environmental toxicants (excluding heavy metals) and children's cognitive, socioemotional, and behavioral development among young children. Methods This literature review highlights research on environmental toxicants (i.e. pesticide exposure, bisphenol A, polycyclic aromatic hydrocarbons, tobacco smoke, polychlorinated biphenyls, flame retardants, phthalates and gas pollutions) and children's development across multiple domains. Results The results highlight the potential risk of exposure to multiple environmental toxicants for young children's cognitive and socioemotional development. Discussion Discussion will focus on the role of environmental toxicants in the cognitive and socioemotional development of young children, while highlighting gaps in the existing literature.

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.

[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.

Exposure to secondhand smoke among adults - Philippines, 2009.

INTRODUCTION: We assessed the differences in exposure to secondhand smoke (SHS) among adults at home, in indoor workplaces, and in various public places in the Philippines across various socio-demographic groups. METHODS: Data from the Global Adult Tobacco Survey conducted in 2009 in the Philippines were used. The data consist of survey answers from 9705 respondents from a nationally representative, multistage probability sample of adults aged 15 years or older. We considered that respondents were exposed to SHS if during the previous 30 days they reported that they lived in a home, worked in a building, or visited a public place where people smoked. The public places included in our analysis were indoor workplaces, public transportation vehicles, restaurants, government buildings or offices, and healthcare facilities. The differences in various socioeconomic and demographic groups' exposure to SHS in these places were also examined. RESULTS: Of respondents who reported working indoors, 36.8% were exposed to SHS. Men (43.3% [95% CI 39.7-46.9]) were more likely than women (28.8% [95% CI 25.4-32.4]) to be exposed to SHS (p < 0.001). Of those working in sites where smoking was not allowed, 13.9% were exposed to SHS, whereas 66.5% were exposed where smoking is allowed in some enclosed areas, and 90.7% were exposed where smoking is allowed everywhere. During the 30 days preceding the survey, more than 50% of those who took public transportation were exposed to SHS; exposure for those who visited public buildings was 33.6% in restaurants, 25.5% in government buildings or offices, and 7.6% in healthcare facilities. CONCLUSION: Despite a national law passed and several local government ordinances that have promulgated smoke-free workplaces, schools, government offices, and healthcare facilities, our findings show that a large proportion of adults were exposed to SHS at work and in public places, which offers opportunities to strengthen and improve enforcement of the smoke-free initiatives and ordinances in the Philippines.

A simplified risk-ranking system for prioritizing toxic pollution sites in low- and middle-income countries.

BACKGROUND: In low- and middle-income countries (LMICs), chemical exposures in the environment due to hazardous waste sites and toxic pollutants are typically poorly documented and their health impacts insufficiently quantified. Furthermore, there often is only limited understanding of the health and environmental consequences of point source pollution problems, and little consensus on how to assess and rank them. The contributions of toxic environmental exposures to the global burden of disease are not well characterized. OBJECTIVES: The aim of this study was to describe the simple but effective approach taken by Blacksmith Institute's Toxic Sites Identification Program to quantify and rank toxic exposures in LMICs. This system is already in use at more than 3000 sites in 48 countries such as India, Indonesia, China, Ghana, Kenya, Tanzania, Peru, Bolivia, Argentina, Uruguay, Armenia, Azerbaijan, and Ukraine. METHODS: A hazard ranking system formula, the Blacksmith Index (BI), takes into account important factors such as the scale of the pollution source, the size of the population possibly affected, and the exposure pathways, and is designed for use reliably in low-resource settings by local personnel provided with limited training. FINDINGS: Four representative case studies are presented, with varying locations, populations, pollutants, and exposure pathways. The BI was successfully applied to assess the extent and severity of environmental pollution problems at these sites. CONCLUSIONS: The BI is a risk-ranking tool that provides direct and straightforward characterization, quantification, and prioritization of toxic pollution sites in settings where time, money, or resources are limited. It will be an important and useful tool for addressing toxic pollution problems in LMICs. Although the BI does not have the sophistication of the US Environmental Protection Agency's Hazard Ranking System, the case studies presented here document the effectiveness of the BI in the field, especially in low-resource settings. Understanding of the risks posed by toxic pollution sites helps assure better use of resources to manage sites and mitigate risks to public health. Quantification of these hazards is an important input to assessments of the global burden of disease.

Environmental influences on systemic lupus erythematosus expression.

The etiology of systemic lupus erythematosus (SLE) is unknown, but multiple genetic, epigenetic, and environmental risk factors have been implicated. The inheritance of genes alone is not sufficient for developing SLE, suggesting the influence of environmental triggers on disease expression. Despite the tremendous amount of progress in elucidating potential environmental risk factors for SLE, much more needs to be done. An interdisciplinary approach to studies of the causes and, ultimately, prevention of SLE is needed. This article reviews what is understood about the epidemiology of the relationship between environmental exposures and SLE, in addition to emerging areas of study.

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.

Relationship between environmental exposure to pesticides and anthropometric outcomes of boys in the rural Western Cape, South Africa.

BACKGROUND: Rural residents in the Western Cape (WC), South Africa (SA) are highly exposed to agricultural pesticides that could impact their reproductive development. However, epidemiological evidence of the effect of pesticides on pubertal growth is contradictory. OBJECTIVE: To investigate the effect of pesticide exposure measured using indices of environmental exposure to pesticides on the pubertal growth of boys in rural WC, SA. METHODS: A cross-sectional study of 269 boys (177 of whom gave a history of residing on farms) was conducted. A questionnaire was administered, height and weight were measured and body mass index was calculated. A proximity index (PI) and spraying index (SI) was developed, measuring the lifetime average home distance from pesticide spraying and average frequency of spraying pesticides on a farm, respectively. RESULTS: Median age of boys was 12.4 years (interquartile range 9.5 - 13.3). More than 60% boys had height and weight <50th percentile for age. After adjusting for confounders, PI was significantly associated with shorter stature and lower weight (-1.7 cm/10-fold decrease, p=0.02 and -1.24 kg/10-fold decrease, p=0.04; respectively) and SI was non-significantly associated (-1.4 cm/10-fold increase, p=0.05 and -1.1 cm/10-fold increase, p=0.06; respectively). Associations were stronger for boys aged <11 years and were weaker when excluding non- farm boys. There were no other associations between outcome and exposure. CONCLUSIONS: The use of quantitative exposure indices showed that lower heights and weights might be associated with pesticide exposure in farm boys v. non-farm boys, but not among farm boys. Lower anthropometric measurements among farm boys v. non-farm boys appear stronger at a younger age. The indices of environmental exposure to pesticides require further development.

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.

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.

Risk factors for age at initial Pseudomonas acquisition in the cystic fibrosis epic observational cohort.

BACKGROUND: Risk factors for initial Pseudomonas aeruginosa (Pa) acquisition, particularly environmental exposures, are poorly understood. We aimed to identify such risk factors in order to inform prevention strategies and identify high-risk populations. METHODS: The study cohort included all participants in the U.S. EPIC Observational Study who had no prior Pa-positive respiratory cultures (N=889). Cox proportional hazard models were used to test the effects of factors on age at first Pa-positive respiratory culture. RESULTS: Cystic fibrosis (CF) genotype functional class had an important effect on age at initial Pa acquisition (hazard ratio (HR) comparing minimal to residual CFTR function 2.87 (95% CI 1.88, 4.39)). None of the modifiable risk factors evaluated, including cigarette smoke, hot tub use, breastfeeding, or daycare, was associated with age at Pa acquisition. Similarly, newborn screening was not associated with age at Pa acquisition (HR 0.85, 95% CI 0.66, 1.09). Key associations were validated in a CF Foundation National Patient Registry replication cohort. CONCLUSIONS: Given the ubiquitous presence of Pa in the environment, it may be that many imposed lifestyle changes will have less impact on age at initial Pa acquisition than genetic determinants.

Estimating the health effects of exposure to multi-pollutant mixture.

PURPOSE: Air pollution constitutes a major public health concern because of its ubiquity and of its potential health impact. Because individuals are exposed to many air pollutants at once that are highly correlated with each other, there is a need to consider the multi-pollutant exposure phenomenon. The characteristics of multiple pollutants that make statistical analysis of health-related effects of air pollution complex include the high correlation between pollutants prevents the use of standard statistical methods, the potential existence of interaction between pollutants, the common measurement errors, the importance of the number of pollutants to consider, and the potential nonlinear relationship between exposure and health. METHODS: We made a review of statistical methods either used in the literature to study the effect of multiple pollutants or identified as potentially applicable to this problem. We reported the results of investigations that applied such methods. RESULTS: Eighteen publications have investigated the multi-pollutant effects, 5 on indoor pollution, 10 on outdoor pollution, and 3 on statistical methodology with application on outdoor pollution. Some other publications have only addressed statistical methodology. CONCLUSIONS: The use of Hierarchical Bayesian approach, dimension reduction methods, clustering, recursive partitioning, and logic regression are some potential methods described. Methods that provide figures for risk assessments should be put forward in public health decisions.