423 research outputs found

    Urinary naphthalene and phenanthrene as biomarkers of occupational exposure to polycyclic aromatic hydrocarbons.

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    OBJECTIVES: The study investigated the utility of unmetabolised naphthalene (Nap) and phenanthrene (Phe) in urine as surrogates for exposures to mixtures of polycyclic aromatic hydrocarbons (PAHs). METHODS: The report included workers exposed to diesel exhausts (low PAH exposure level, n = 39) as well as those exposed to emissions from asphalt (medium PAH exposure level, n = 26) and coke ovens (high PAH exposure level, n = 28). Levels of Nap and Phe were measured in urine from each subject using head space-solid phase microextraction and gas chromatography-mass spectrometry. Published levels of airborne Nap, Phe and other PAHs in the coke-producing and aluminium industries were also investigated. RESULTS: In post-shift urine, the highest estimated geometric mean concentrations of Nap and Phe were observed in coke-oven workers (Nap: 2490 ng/l; Phe: 975 ng/l), followed by asphalt workers (Nap: 71.5 ng/l; Phe: 54.3 ng/l), and by diesel-exposed workers (Nap: 17.7 ng/l; Phe: 3.60 ng/l). After subtracting logged background levels of Nap and Phe from the logged post-shift levels of these PAHs in urine, the resulting values (referred to as ln(adjNap) and ln(adjPhe), respectively) were significantly correlated in each group of workers (0.71 < or = Pearson r < or = 0.89), suggesting a common exposure source in each case. Surprisingly, multiple linear regression analysis of ln(adjNap) on ln(adjPhe) showed no significant effect of the source of exposure (coke ovens, asphalt and diesel exhaust) and further suggested that the ratio of urinary Nap/Phe (in natural scale) decreased with increasing exposure levels. These results were corroborated with published data for airborne Nap and Phe in the coke-producing and aluminium industries. The published air measurements also indicated that Nap and Phe levels were proportional to the levels of all combined PAHs in those industries. CONCLUSION: Levels of Nap and Phe in urine reflect airborne exposures to these compounds and are promising surrogates for occupational exposures to PAH mixtures

    Cumulative ultraviolet radiation flux in adulthood and risk of incident skin cancers in women

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    Background: Solar ultraviolet (UV) exposure estimated based on residential history has been used as a sun exposure indicator in previous case–control and descriptive studies. However, the associations of cumulative UV exposure based on residential history with different skin cancers, including melanoma, squamous cell carcinoma (SCC), and basal cell carcinoma (BCC), have not been evaluated simultaneously in prospective studies. Methods: We conducted a cohort study among 108 578 women in the Nurses' Health Study (1976–2006) to evaluate the relative risks of skin cancers with cumulative UV flux based on residential history in adulthood. Results: Risk of SCC and BCC was significantly lower for women in lower quintiles vs the highest quintile of cumulative UV flux (both P for trend <0.0001). The association between cumulative UV flux and risk of melanoma did not reach statistical significance. However, risk of melanoma appeared to be lower among women in lower quintiles vs the highest quintile of cumulative UV flux in lag analyses with 2–10 years between exposure and outcome. The multivariable-adjusted hazard ratios per 200 × 10−4 Robertson–Berger units increase in cumulative UV flux were 0.979 (95% confidence interval (CI): 0.933, 1.028) for melanoma, 1.072 (95% CI: 1.041, 1.103) for SCC, and 1.043 (95% CI: 1.034, 1.052) for BCC. Conclusions: Associations with cumulative UV exposure in adulthood among women differed for melanoma, SCC, and BCC, suggesting a potential variable role of UV radiation in adulthood in the carcinogenesis of the three major skin cancers

    “Exposure Track”—The Impact of Mobile-Device-Based Mobility Patterns on Quantifying Population Exposure to Air Pollution

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    Air pollution is now recognized as the world’s single largest environmental and human health threat. Indeed, a large number of environmental epidemiological studies have quantified the health impacts of population exposure to pollution. In previous studies, exposure estimates at the population level have not considered spatially- and temporally varying populations present in study regions. Therefore, in the first study of it is kind, we use measured population activity patterns representing several million people to evaluate population-weighted exposure to air pollution on a city-wide scale. Mobile and wireless devices yield information about where and when people are present, thus collective activity patterns were determined using counts of connections to the cellular network. Population-weighted exposure to PM2.5 in New York City (NYC), herein termed “Active Population Exposure” was evaluated using population activity patterns and spatiotemporal PM2.5 concentration levels, and compared to “Home Population Exposure”, which assumed a static population distribution as per Census data. Areas of relatively higher population-weighted exposures were concentrated in different districts within NYC in both scenarios. These were more centralized for the “Active Population Exposure” scenario. Population-weighted exposure computed in each district of NYC for the “Active” scenario were found to be statistically significantly (p < 0.05) different to the “Home” scenario for most districts. In investigating the temporal variability of the “Active” population-weighted exposures determined in districts, these were found to be significantly different (p < 0.05) during the daytime and the nighttime. Evaluating population exposure to air pollution using spatiotemporal population mobility patterns warrants consideration in future environmental epidemiological studies linking air quality and human health

    Racial, Ethnic, and Socioeconomic Disparities in Multiple Measures of Blue and Green Spaces in the United States

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    BACKGROUND: Several studies have evaluated whether the distribution of natural environments differs between marginalized and privileged neighborhoods. However, most studies restricted their analyses to a single or handful of cities and used different natural environment measures. OBJECTIVES: We evaluated whether natural environments are inequitably distributed based on socioeconomic status (SES) and race/ethnicity in the contiguous United States. METHODS: We obtained SES and race/ethnicity data (2015–2019) for all U.S. Census tracts. For each tract, we calculated the Normalized Different Vegetation Index (NDVI) for 2020, NatureScore (a proprietary measure of the quantity and quality of natural elements) for 2019, park cover for 2020, and blue space for 1984–2018. We used generalized additive models with adjustment for potential confounders and spatial autocorrelation to evaluate associations of SES and race/ethnicity with NDVI, NatureScore, park cover, and odds of containing blue space in all tracts ([Formula: see text]) and in urban tracts ([Formula: see text]). To compare effect estimates, we standardized NDVI, NatureScore, and park cover so that beta coefficients presented a percentage increase or decrease of the standard deviation (SD). RESULTS: Tracts with higher SES had higher NDVI, NatureScore, park cover, and odds of containing blue space. For example, urban tracts in the highest median household income quintile had higher NDVI [44.8% of the SD (95% CI: 42.8, 46.8)] and park cover [16.2% of the SD (95% CI: 13.5, 19.0)] compared with urban tracts in the lowest median household income quintile. Across all tracts, a lower percentage of non-Hispanic White individuals and a higher percentage of Hispanic individuals were associated with lower NDVI and NatureScore. In urban tracts, we observed weak positive associations between percentage non-Hispanic Black and NDVI, NatureScore, and park cover; we did not find any clear associations for percentage Hispanics. DISCUSSION: Multiple facets of the natural environment are inequitably distributed in the contiguous United States. https://doi.org/10.1289/EHP1116

    Media, Capabilities, and Justification

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    In this paper, I evaluate the ‘capability approach’ developed by Amartya Sen and Martha Nussbaum as a normative perspective for critical media research. The concept of capabilities provides a valuable way of assessing media and captures important aspects of the relationship between media and equality. However, following Rainer Forst’s critique of outcome- oriented approaches to justice, I argue the capability approach needs to pay more attention to questions of power and process. In particular, when it comes to deciding which capabilities media should promote and what media structure and practices should promote them, the capability approach must accept the priority of deliberative and democratic processes of justification. Once we do this, we are urged to situate the concept of capabilities within a more process-oriented view of justice, focused not on capabilities as such, but on outlining the conditions required for justificatory equality. After discussing the capability approach, I will outline the process-oriented theory of justice Forst has developed around the idea of the ‘right to justification’. While Forst does not discuss media in depth, I argue his theory of justice can provide a valuable alternative normative standpoint for the critical media research

    The Diesel Exhaust in Miners Study: A Nested Case–Control Study of Lung Cancer and Diesel Exhaust

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    BACKGROUND Most studies of the association between diesel exhaust exposure and lung cancer suggest a modest, but consistent, increased risk. However, to our knowledge, no study to date has had quantitative data on historical diesel exposure coupled with adequate sample size to evaluate the exposure-response relationship between diesel exhaust and lung cancer. Our purpose was to evaluate the relationship between quantitative estimates of exposure to diesel exhaust and lung cancer mortality after adjustment for smoking and other potential confounders. METHODS We conducted a nested case-control study in a cohort of 12 315 workers in eight non-metal mining facilities, which included 198 lung cancer deaths and 562 incidence density-sampled control subjects. For each case subject, we selected up to four control subjects, individually matched on mining facility, sex, race/ethnicity, and birth year (within 5 years), from all workers who were alive before the day the case subject died. We estimated diesel exhaust exposure, represented by respirable elemental carbon (REC), by job and year, for each subject, based on an extensive retrospective exposure assessment at each mining facility. We conducted both categorical and continuous regression analyses adjusted for cigarette smoking and other potential confounding variables (eg, history of employment in high-risk occupations for lung cancer and a history of respiratory disease) to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Analyses were both unlagged and lagged to exclude recent exposure such as that occurring in the 15 years directly before the date of death (case subjects)/reference date (control subjects). All statistical tests were two-sided. RESULTS We observed statistically significant increasing trends in lung cancer risk with increasing cumulative REC and average REC intensity. Cumulative REC, lagged 15 years, yielded a statistically significant positive gradient in lung cancer risk overall (P (trend) = .001); among heavily exposed workers (ie, above the median of the top quartile [REC ≥ 1005 μg/m(3)-y]), risk was approximately three times greater (OR = 3.20, 95% CI = 1.33 to 7.69) than that among workers in the lowest quartile of exposure. Among never smokers, odd ratios were 1.0, 1.47 (95% CI = 0.29 to 7.50), and 7.30 (95% CI = 1.46 to 36.57) for workers with 15-year lagged cumulative REC tertiles of less than 8, 8 to less than 304, and 304 μg/m(3)-y or more, respectively. We also observed an interaction between smoking and 15-year lagged cumulative REC (P (interaction) = .086) such that the effect of each of these exposures was attenuated in the presence of high levels of the other. CONCLUSION Our findings provide further evidence that diesel exhaust exposure may cause lung cancer in humans and may represent a potential public health burden

    Long-term particulate matter exposure and mortality: a review of European epidemiological studies

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    <p>Abstract</p> <p>Background</p> <p>Several studies considered the relation between long-term exposure to particulate matter (PM) and total mortality, as well as mortality from cardiovascular and respiratory diseases. Our aim was to provide a comprehensive review of European epidemiological studies on the issue.</p> <p>Methods</p> <p>We searched the Medline database for epidemiological studies on air pollution and health outcomes published between January 2002 and December 2007. We also examined the reference lists of individual papers and reviews. Two independent reviewers classified the studies according to type of air pollutant, duration of exposure and health outcome considered. Among European investigations that examined long-term PM exposure we found 4 cohort studies (considering total and cardiopulmonary mortality), 1 case-control study (considering mortality from myocardial infarction), and 4 ecologic studies (2 studies considering total and cardiopulmonary mortality and 2 studies focused on cardiovascular mortality).</p> <p>Results</p> <p>Measurement indicators of PM exposure used in European studies, including PM10, PM2.5, total suspended particulate and black smoke, were heterogeneous. This notwithstanding, in all analytic studies total mortality was directly associated with long-term exposure to PM. The excesses in mortality were mainly due to cardiovascular and respiratory causes. Three out of 4 ecologic studies found significant direct associations between PM indexes and mortality.</p> <p>Conclusion</p> <p>European studies on long-term exposure to PM indicate a direct association with mortality, particularly from cardiovascular and respiratory diseases.</p

    How to determine life expectancy change of air pollution mortality: a time series study

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    <p>Abstract</p> <p>Background</p> <p>Information on life expectancy (LE) change is of great concern for policy makers, as evidenced by discussions of the "harvesting" (or "mortality displacement") issue, i.e. how large an LE loss corresponds to the mortality results of time series (TS) studies. Whereas loss of LE attributable to chronic air pollution exposure can be determined from cohort studies, using life table methods, conventional TS studies have identified only deaths due to acute exposure, during the immediate past (typically the preceding one to five days), and they provide no information about the LE loss per death.</p> <p>Methods</p> <p>We show how to obtain information on population-average LE loss by extending the observation window (largest "lag") of TS to include a sufficient number of "impact coefficients" for past exposures ("lags"). We test several methods for determining these coefficients. Once all of the coefficients have been determined, the LE change is calculated as time integral of the relative risk change after a permanent step change in exposure.</p> <p>Results</p> <p>The method is illustrated with results for daily data of non-accidental mortality from Hong Kong for 1985 - 2005, regressed against PM<sub>10 </sub>and SO<sub>2 </sub>with observation windows up to 5 years. The majority of the coefficients is statistically significant. The magnitude of the SO<sub>2 </sub>coefficients is comparable to those for PM<sub>10</sub>. But a window of 5 years is not sufficient and the results for LE change are only a lower bound; it is consistent with what is implied by other studies of long term impacts.</p> <p>Conclusions</p> <p>A TS analysis can determine the LE loss, but if the observation window is shorter than the relevant exposures one obtains only a lower bound.</p
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