Residential exposure to traffic pollution and mammographic density in premenopausal women.

BACKGROUND: Mammographic density (MD) is the most important breast cancer biomarker. Ambient pollution is a carcinogen, and its relationship with MD is unclear. This study aims to explore the association between exposure to traffic pollution and MD in premenopausal women. METHODOLOGY: This Spanish cross-sectional study involved 769 women attending gynecological examinations in Madrid. Annual Average Daily Traffic (AADT), extracted from 1944 measurement road points provided by the City Council of Madrid, was weighted by distances (d) between road points and women's addresses to develop a Weighted Traffic Exposure Index (WTEI). Three methods were employed: method-1 (1dAADT), method-2 (1dAADT), and method-3 (e1dAADT). Multiple linear regression models, considering both log-transformed percentage of MD and untransformed MD, were used to estimate MD differences by WTEI quartiles, through two strategies: "exposed (exposure buffers between 50 and 200 m) vs. not exposed (>200 m)"; and "degree of traffic exposure". RESULTS: Results showed no association between MD and traffic pollution according to buffers of exposure to the WTEI (first strategy) for the three methods. The highest reductions in MD, although not statistically significant, were detected in the quartile with the highest traffic exposure. For instance, method-3 revealed a suggestive inverse trend (eßQ1 = 1.23, eßQ2 = 0.96, eßQ3 = 0.85, eßQ4 = 0.85, p-trend = 0.099) in the case of 75 m buffer. Similar non-statistically significant trends were observed with Methods-1 and -2. When we examined the effect of traffic exposure considering all the 1944 measurement road points in every participant (second strategy), results showed no association for any of the three methods. A slightly decreased MD, although not significant, was observed only in the quartile with the highest traffic exposure: eßQ4 = 0.98 (method-1), and eßQ4 = 0.95 (methods-2 and -3). CONCLUSIONS: Our results showed no association between exposure to traffic pollution and MD in premenopausal women. Further research is needed to validate these findings.

Effect of heavy metals on ventricular repolarization and depolarization in the Metropolitan Manila Development Authority (MMDA) traffic enforcers' health study.

We examined the relationships between blood heavy metals [cadmium (B-Cd), mercury (B-Hg), and lead (B-Pb)] and heart rate-corrected QT interval (QTc), JT interval (JTc), and QRS complex duration (QRSc), electrocardiogram markers of ventricular repolarization and depolarization among 60 traffic enforcers in the MMDA traffic enforcers' health study. We fitted regression models to estimate the mean change effect on QTc, JTc, and QRSc, of B-Cd, B-Hg, and B-Pb concentrations, adjusted for potential confounding factors. We looked at effect modification by sex and smoking status. An interquartile range increase in B-Cd (0.9 µg/L) was related to a 6.6% increase in mean QRSc [95% confidence interval (CI): 2.5, 10.8], and a 1.7% increase in mean QTc (95% CI: 0.2, 3.3). We also found that the associations between B-Cd and QRSc and QTc were higher among participants who were never smokers than ever smokers. Moreover, the association between B-Cd and QRSc was also higher among males than females.

Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

BACKGROUND: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures. METHODS: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status. RESULTS: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5. CONCLUSION: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.

Acute cardiovascular health effects in a panel study of personal exposure to traffic-related air pollutants and noise in Toronto, Canada.

Urban populations are often simultaneously exposed to air pollution and environmental noise, which are independently associated with cardiovascular disease. Few studies have examined acute physiologic responses to both air and noise pollution using personal exposure measures. We conducted a repeated measures panel study of air pollution and noise in 46 non-smoking adults in Toronto, Canada. Data were analyzed using linear mixed-effects models and weighted cumulative exposure modeling of recent exposure. We examined acute changes in cardiovascular health effects of personal (ultrafine particles, black carbon) and regional (PM2.5, NO2, O3, Ox) measurements of air pollution and the role of personal noise exposure as a confounder of these associations. We observed adverse changes in subclinical cardiovascular outcomes in response to both air pollution and noise, including changes in endothelial function and heart rate variability (HRV). Our findings show that personal noise exposures can confound associations for air pollutants, particularly with HRV, and that impacts of air pollution and noise on HRV occur soon after exposure. Thus, both noise and air pollution have a measurable impact on cardiovascular physiology. Noise should be considered alongside air pollution in future studies to elucidate the combined impacts of these exposures in urban environments.

Traffic-Related Air Pollution and Carotid Plaque Burden in a Canadian City With Low-Level Ambient Pollution.

Background The association between fine particulate matter and cardiovascular disease has been convincingly demonstrated. The role of traffic-related air pollutants is less clear. To better understand the role of traffic-related air pollutants in cardiovascular disease development, we examined associations between NO2, carotid atherosclerotic plaque, and cardiometabolic disorders associated with cardiovascular disease. Methods and Results Cross-sectional analyses were conducted among 2227 patients (62.9±13.8 years; 49.5% women) from the Stroke Prevention and Atherosclerosis Research Centre (SPARC) in London, Ontario, Canada. Total carotid plaque area measured by ultrasound, cardiometabolic disorders, and residential locations were provided by SPARC medical records. Long-term outdoor residential NO2 concentrations were generated by a land use regression model. Associations between NO2, total carotid plaque area, and cardiometabolic disorders were examined using multiple regression models adjusted for age, sex, smoking, and socioeconomic status. Mean NO2 was 5.4±1.6 ppb in London, Ontario. NO2 was associated with a significant increase in plaque (3.4 mm2 total carotid plaque area per 1 ppb NO2), exhibiting a linear dose-response. NO2 was also positively associated with triglycerides, total cholesterol, and the ratio of low- to high-density lipoprotein cholesterol (P<0.05). Diabetes mellitus mediated the relationship between NO2 and total carotid plaque area (P<0.05). Conclusions Our results demonstrate that even low levels of traffic-related air pollutants are linked to atherosclerotic plaque burden, an association that may be partially attributable to pollution-induced diabetes mellitus. Our findings suggest that reducing ambient concentrations in cities with NO2 below current standards would result in additional health benefits. Given the billions of people exposed to traffic emissions, our study supports the global public health significance of reducing air pollution.

Biomarkers of exposure, effect, and susceptibility in occupational exposure to traffic-related air pollution: A review.

There is a well-recognized association between environmental air pollution exposure and several human diseases. However, the relationship between diseases related to occupational air pollution exposure on roads and high levels of traffic-related air pollutants (TRAPs) is less substantiated. Biomarkers are essential tools in environmental and occupational toxicology, and studies on new biomarkers are increasingly relevant due to the need to determine early biomarkers to be assessed in exposure conditions. This review aimed to investigate the main advances in the biomonitoring of subjects occupationally exposed to air pollution, as well as to summarize the biomarkers of exposure, effect, and susceptibility. Furthermore, we discuss how biomarkers could be used to complement the current application of methods used to assess occupational exposures to xenobiotics present in air pollution. The databases used in the preparation of this review were PubMed, Scopus, and Science Direct. Considering the significant deleterious effects on health associated with chronic occupational exposure to xenobiotics, this topic deserves attention. As it is difficult to avoid occupational exposure to TRAPs, biomonitoring should be applied as a strategy to reduce the toxic effects of workplace exposure.

Surrounding green, air pollution, traffic noise exposure and non-accidental and cause-specific mortality.

BACKGROUND: Most previous studies that investigated associations of surrounding green, air pollution or traffic noise with mortality focused on single exposures. OBJECTIVES: The aim of this study was to evaluate combined associations of long-term residential exposure to surrounding green, air pollution and traffic noise with total non-accidental and cause-specific mortality. METHODS: We linked a national health survey (Public Health Monitor, PHM) conducted in 2012 to the Dutch longitudinal mortality database. Subjects of the survey who were 30 years or older on 1 January 2013 (n = 339,633) were followed from 1 January 2013 till 31 December 2017. We used Cox proportional hazard models to evaluate associations of residential surrounding green (including the average Normalized Difference Vegetation Index (NDVI) in buffers of 300 m and 1000 m), annual average air pollutant concentrations (including particulate matter (PM10, PM2.5), nitrogen dioxide (NO2)) and traffic noise with non-accidental, circulatory disease, respiratory disease, lung cancer and neurodegenerative disease mortality. RESULTS: We observed 26,886 non-accidental deaths over 1.627.365 person-years of follow-up. Surrounding green, air pollution and traffic noise exposure were not significantly associated with non-accidental or cause-specific mortality. For non-accidental mortality, we found a hazard ratio (HR) of 0.99 (0.98, 1.01) per IQR increase in NDVI 300 m, a HR of 0.99 (95% CI: 0.97, 1.01) per IQR increase in NO2, a HR of 0.98 (0.97, 1.00) per IQR increase in PM2.5 and a HR of 0.99 (95% CI: 0.97, 1.01) per IQR increase in road-traffic noise. Analyses restricted to non-movers or excluding subjects aged 85+ years did not change the findings. CONCLUSION: We found no evidence for associations of long-term residential exposures to surrounding green, air pollution and traffic noise with non-accidental or cause-specific mortality in a large population based survey in the Netherlands, possibly related to the relatively short follow-up period.

Evaluation of the exposure, dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos in a 90-day quantitative inhalation toxicology study - Interim results Part 1: Experimental design, aerosol exposure, lung burdens and BAL.

This 90-day repeated-dose inhalation toxicology study of brake-dust (BD) (brakes manufactured with chrysotile) in rats provides a comprehensive understanding of the biokinetics and potential toxicology in the lung and pleura. Exposure was 6 h/d, 5d/wk., 13wks followed by lifetime observation (~20 % survival). Control groups included a particle control (TiO2), chrysotile, commercial crocidolite and amosite asbestos. Aerosol fiber distributions of the chrysotile, crocidolite and amosite were similar (fibers L > 20 µm/cm3: chrysotile-Low/High 29/72; crocidolite 24; amosite 47 fibers/cm3; WHO-fibers/cm3: chrysotile-Low/High 119/233; crocidolite 181; amosite 281 fibers/cm3). The number of particles/cm3 in the BD was similar to that in the chrysotile, crocidolite & amosite exposures (BD 470-715; chrysotile 495-614; crocidolite 415; amosite 417 particles/cm3). In the BD groups, few fibers L > 20 µm were observed in the lungs at the end of exposure and no fibers L > 20 µm at 90d post exposure. In the chrysotile groups, means of 204,000 and 290,000 fibers(L > 20 µm)/lung were measured at 89d. By 180d, means of 1 and 3.9 fibers were counted on the filter corresponding to 14,000 and 55,000 fibers(L > 20 µm)/lung. In the crocidolite and amosite groups mean lung concentrations were 9,055,000 and 11,645,000 fibers(L > 20 µm)/lung at 89d. At 180d the means remained similar with 8,026,000 and 11,591,000 fibers(L > 20 µm)/lung representing 10-13% of the total lung fibers. BAL determined the total number of macrophages, lymphocytes, neutrophils, eosinophils, epithelial-cells and IL-1 beta, TNF-alpha and TGF-beta. At the moderate aerosol concentrations used in this study, neutrophil counts increased ~5 fold in the amphibole asbestos exposure groups. All other groups and parameters showed no important differences at these exposure concentrations. The exposure and lung burden results provide a sound basis for assessing the potential toxicity of the brake dust in comparison to the TiO2 particle control and the chrysotile, crocidolite and amosite asbestos control groups. The BAL results provide an initial indication of the differential response. Part 2 presents the presentation and discussion of the histopathological and confocal microscopy findings in this study through 90 days post exposure.

Evaluation of the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos in a 90-day quantitative inhalation toxicology study - Interim results Part 2: Histopathological examination, Confocal microscopy and collagen quantification of the lung and pleural cavity.

The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

Self-reported traffic-related air pollution and respiratory symptoms among adults in an area with modest levels of traffic.

Health effects of traffic-related air pollution (TRAP) concentrations in densely populated areas are previously described. However, there is still a lack of knowledge of the health effects of moderate TRAP levels. The aim of the current study, a population-based survey including 16 099 adults (response rate 33%), was to assess the relationship between TRAP estimates and respiratory symptoms in an area with modest levels of traffic; Telemark County, Norway. Respondents reported respiratory symptoms the past 12 months and two TRAP exposure estimates: amount of traffic outside their bedroom window and time spent by foot daily along a moderate to heavy traffic road. Females reported on average more symptoms than males. Significant relationships between traffic outside their bedroom window and number of symptoms were only found among females, with the strongest associations among female occasional smokers (incidence rate ratio [IRR], 1.75, 95% confidence interval (CI) [1.16-2.62] for moderate or heavy traffic compared to no traffic). Significant relationship between time spent daily by foot along a moderate to heavy traffic road and number of symptoms was found among male daily smokers (IRR 1.09, 95% CI [1.04-1.15] per hour increase). Associations between traffic outside bedroom window and each respiratory symptom were found. Significant associations were primarily detected among females, both among smokers and non-smokers. Significant associations between time spent by foot daily along a moderate to heavy traffic road (per hour) and nocturnal dyspnoea (odds ratio (OR) 1.20, 95% CI [1.05-1.38]), nocturnal chest tightness (OR 1.13 [1.00-1.28]) and wheezing (OR 1.14 [1.02-1.29]) were found among daily smokers, primarily men. Overall, we found significant associations between self-reported TRAP exposures and respiratory symptoms. Differences between genders and smoking status were identified. The findings indicate an association between TRAP and respiratory symptoms even in populations exposed to modest levels of TRAP.

Air Pollution in Kazakhstan and Its Health Risk Assessment.

Background: Air pollution in Kazakhstan is caused by many factors and poses serious threats to public health. Ambient air in the cities of Kazakhstan is polluted due to mining and processing of mineral resources, oil and gas production, gasoline and diesel fuel motor vehicles, industrial enterprises. Objective: The study aim is to assess the air pollution degree in most significant settlements of Kazakhstan and define risk levels for the population health. Ambient air monitoring was conducted in 26 cities. Air pollution severity was assessed by the analysis results and processing of air samples taken at the stationary observation posts. Health risk assessment due to chemical factors was calculated according to the approved risk assessment methodology. Findings: There is high risk of acute adverse effects risk from suspended particles, oxides and dioxides of nitrogen and sulfur in almost all of the studied cities. The most unfavorable situation is in Ust-Kamenogorsk. Also, there is the adverse chronic effects risk caused by suspended particles exposure in majority of the studied cities. Extremely high chronic effects risk as a result of heavy metals exposure was detected in Ust-Kamenogorsk, Shymkent, Almaty, Taraz and Balkhash. Unacceptable carcinogenic risk levels have been determined for professional groups and the whole population with respect to cadmium in Shymkent, Almaty, Balkhash; arsenic in Shymkent, Almaty, Balkhash; lead in Taraz; chromium - in Shymkent, Aktobe, Almaty and Balkhash. Thus, the values of the hazard quotients and indices for acute and chronic exposure in most of the studied cities of Kazakhstan exceed the permissible level equal to 1.0. Conclusion: Due to the unacceptable risk levels in the cities it is strongly recommended to conduct a detailed study of the health status of the population depending on the air pollution.

Ambient air pollution exposure and risk and progression of interstitial lung abnormalities: the Framingham Heart Study.

BACKGROUND: Ambient air pollution accelerates lung function decline among adults, however, there are limited data about its role in the development and progression of early stages of interstitial lung disease. AIMS: To evaluate associations of long-term exposure to traffic and ambient pollutants with odds of interstitial lung abnormalities (ILA) and progression of ILA on repeated imaging. METHODS: We ascertained ILA on chest CT obtained from 2618 Framingham participants from 2008 to 2011. Among 1846 participants who also completed a cardiac CT from 2002 to 2005, we determined interval ILA progression. We assigned distance from home address to major roadway, and the 5-year average of fine particulate matter (PM2.5), elemental carbon (EC, a traffic-related PM2.5 constituent) and ozone using spatio-temporal prediction models. Logistic regression models were adjusted for age, sex, body mass index, smoking status, packyears of smoking, household tobacco exposure, neighbourhood household value, primary occupation, cohort and date. RESULTS: Among 2618 participants with a chest CT, 176 (6.7%) had ILA, 1361 (52.0%) had no ILA, and the remainder were indeterminate. Among 1846 with a preceding cardiac CT, 118 (6.4%) had ILA with interval progression. In adjusted logistic regression models, an IQR difference in 5-year EC exposure of 0.14 µg/m3 was associated with a 1.27 (95% CI 1.04 to 1.55) times greater odds of ILA, and a 1.33 (95% CI 1.00 to 1.76) times greater odds of ILA progression. PM2.5 and O3 were not associated with ILA or ILA progression. CONCLUSIONS: Exposure to EC may increase risk of progressive ILA, however, associations with other measures of ambient pollution were inconclusive.

Supplemental Folate and the Relationship Between Traffic-Related Air Pollution and Livebirth Among Women Undergoing Assisted Reproduction.

Traffic-related air pollution has been linked to higher risks of infertility and miscarriage. We evaluated whether folate intake modified the relationship between air pollution and livebirth among women using assisted reproductive technology (ART). Our study included 304 women (513 cycles) presenting to a fertility center in Boston, Massachusetts (2005-2015). Diet and supplements were assessed by food frequency questionnaire. Spatiotemporal models estimated residence-based daily nitrogen dioxide (NO2), ozone, fine particulate, and black carbon concentrations in the 3 months before ART. We used generalized linear mixed models with interaction terms to evaluate whether the associations between air pollutants and livebirth were modified by folate intake, adjusting for age, body mass index, race, smoking, education, infertility diagnosis, and ART cycle year. Supplemental folate intake significantly modified the association of NO2 exposure and livebirth (P = 0.01). Among women with supplemental folate intakes of <800 µg/day, the odds of livebirth were 24% (95% confidence interval: 2, 42) lower for every 20-parts-per-billion increase in NO2 exposure. There was no association among women with intakes of ≥800 µg/day. There was no effect modification of folate on the associations between other air pollutants and livebirth. High supplemental folate intake might protect against the adverse reproductive consequences of traffic-related air pollution.

Combustion Particle-Induced Changes in Calcium Homeostasis: A Contributing Factor to Vascular Disease?

Air pollution is the leading environmental risk factor for disease and premature death in the world. This is mainly due to exposure to urban air particle matter (PM), in particular, fine and ultrafine combustion-derived particles (CDP) from traffic-related air pollution. PM and CDP, including particles from diesel exhaust (DEP), and cigarette smoke have been linked to various cardiovascular diseases (CVDs) including atherosclerosis, but the underlying cellular mechanisms remain unclear. Moreover, CDP typically consist of carbon cores with a complex mixture of organic chemicals such as polycyclic aromatic hydrocarbons (PAHs) adhered. The relative contribution of the carbon core and adhered soluble components to cardiovascular effects of CDP is still a matter of discussion. In the present review, we summarize evidence showing that CDP affects intracellular calcium regulation, and argue that CDP-induced impairment of normal calcium control may be a critical cellular event through which CDP exposure contributes to development or exacerbation of cardiovascular disease. Furthermore, we highlight in vitro research suggesting that adhered organic chemicals such as PAHs may be key drivers of these responses. CDP, extractable organic material from CDP (CDP-EOM), and PAHs may increase intracellular calcium levels by interacting with calcium channels like transient receptor potential (TRP) channels, and receptors such as G protein-coupled receptors (GPCR; e.g., beta-adrenergic receptors [ßAR] and protease-activated receptor 2 [PAR-2]) and the aryl hydrocarbon receptor (AhR). Clarifying a possible role of calcium signaling and mechanisms involved may increase our understanding of how air pollution contributes to CVD.

A Meta-analysis of Traffic-related Air Pollution and Risk of Childhood Leukemia.

BACKGROUND: Many studies have analyzed the association between traffic-related air pollution and risk of childhood leukemia, but the results are inconsistent. Therefore, we performed this meta-analysis to investigate the association between traffic-related air pollution and risk of childhood leukemia. METHODS: PubMed, Cochrane, and Embase databases were searched by the index words to identify eligible case-control studies, and relevant literature sources were also searched. The latest research was performed in September 2017. Odds ratio (OR) along with 95% confidence interval (95% CI) were used to analyzed the main outcomes. RESULTS: Twenty-one case-control studies were included in the meta-analysis. The results indicated that in the studies of overall traffic density (OR: 1.01, 95% CI: 0.98-1.04), high traffic density (OR: 1.04, 95% CI: 0.91-1.17), moderate exposure to NO2 (OR: 1.02, 95% CI: 0.93-1.10), and benzene (OR: 1.04, 95% CI: 0.71-1.37), the risks of childhood leukemia incidence were higher in the case group than the control group, but no significant difference was found. In other analysis, no significant difference was observed in the risk of childhood leukemia in the 2 groups. CONCLUSIONS: Current evidence suggests that childhood leukemia is associated with traffic density, and moderate exposure to NO2 and benzene. However, more high-quality studies are required to confirm the conclusions.

Multicentre, population-based, case-control study of particulates, combustion products and amyotrophic lateral sclerosis risk.

OBJECTIVE: To investigate whether exposure to particulates and combustion products may explain the association between certain occupations and amyotrophic lateral sclerosis (ALS) risk in a large, multicentre, population-based, case-control study, based on full job histories, using job-exposure matrices, with detailed information on possible confounders. METHODS: Population-based patients with ALS and controls were recruited from five registries in the Netherlands, Ireland and Italy. Demographics and data regarding educational level, smoking, alcohol habits and lifetime occupational history were obtained using a validated questionnaire. Using job-exposure matrices, we assessed occupational exposure to silica, asbestos, organic dust, contact with animals or fresh animal products, endotoxins, polycyclic aromatic hydrocarbons and diesel motor exhaust. Multivariate logistic regression models adjusting for confounding factors were used to determine the association between these exposures and ALS risk. RESULTS: We included 1557 patients and 2922 controls. Associations were positive for all seven occupational exposures (ORs ranging from 1.13 to 1.73 for high vs never exposed), and significant on the continuous scale for silica, organic dust and diesel motor exhaust (p values for trend ≤0.03). Additional analyses, adding an exposure (one at a time) to the model in the single exposure analysis, revealed a stable OR for silica. We found similar results when patients with a C9orf72 mutation were excluded. CONCLUSION: In a large, multicentre study, using harmonised methodology to objectively quantify occupational exposure to particulates and combustion products, we found an association between ALS risk and exposure to silica, independent of the other occupational exposures studied.

[Influence of vehicular traffic density on hospital admissions due to respiratory tract cancer in the city of São Paulo, Brazil]. / Influência da densidade de tráfego veicular na internação por câncer do aparelho respiratório no Município de São Paulo, Brasil.

Pollution related to traffic is a major problem in urban centers and a large portion of the population is vulnerable to its health effects. This study sought to identify a potential association between hospital admissions due to respiratory tract cancer and vehicular traffic density in the city of São Paulo, Brazil. It is an ecological study of the public (Hospital Inpatient Authorization - AIH, in Portuguese) and private (Hospital Inpatient Communication - CIH, in Portuguese) health care systems, from 2004 to 2006, geocoded by individuals' residential addresses. Using a Besag-York-Mollié ecological model, we initially evaluated the relationship between number of cases of hospital admission due to respiratory tract cancer in each weighting area and the standardized co-variables: traffic density and Municipal Human Development Index (MHDI) as indicator of socioeconomic status. Using a classic Poisson model, we then evaluated the risk associated with growing traffic density categories. The Besag-York-Mollié model estimated a RR = 1.09 (95%CI: 1.02-1.15) and RR = 1.19 (95%CI: 1.10-1.29) of admission due to respiratory tract cancer for each increase of one standard deviation of traffic and MHDI, respectively. The Poisson model also showed a clear exposure-response gradient for admission due to respiratory tract cancer (IRR = 1.11; 95%CI: 1.07-1.15, for each 10 units of added traffic density). This study suggests that there is an association between residing in areas with high traffic density and hospital admissions due to respiratory tract cancer in the city of São Paulo.

A poluição relacionada ao tráfego é um grande problema nos centros urbanos, e uma grande parcela da população fica vulnerável aos seus efeitos à saúde. Este trabalho teve como objetivo identificar potencial associação entre as internações hospitalares por câncer do aparelho respiratório com a densidade de tráfego veicular no Município de São Paulo, Brasil. É um estudo ecológico com dados de internações hospitalares por câncer dos sistemas público (Autorização de Internação Hospitalar - AIH) e particular (Comunicação de Internação Hospitalar - CIH), de 2004 a 2006, geocodificados por endereço de residência do indivíduo. Mediante um modelo ecológico de Besag-York-Mollié foi avaliada inicialmente a relação entre o número de casos de internação por câncer do aparelho respiratório em cada área de ponderação e as covariáveis padronizadas: densidade de tráfego e Índice de Desenvolvimento Humano Municipal (IDHM) como indicador de status socioeconômico. Sequencialmente, com um modelo clássico de Poisson, procedeu-se uma avaliação do risco associado às categorias crescentes de densidade de tráfego. O modelo de Besag-York-Mollié estimou um RR = 1,09 (IC95%: 1,02-1,15) e RR = 1,19 (IC95%: 1,10-1,29) de internação por câncer do aparelho respiratório, para cada aumento de um desvio padrão da densidade de tráfego e IDHM, respectivamente. Foi também evidenciado pelo modelo de Poisson um claro gradiente de exposição-resposta para internação por câncer respiratório (IRR = 1,11; IC95%: 1,07-1,15, para cada dez unidades de acréscimo da densidade de tráfego). Este trabalho sugere que há associação entre residir em áreas com alta densidade de tráfego e internação por câncer do aparelho respiratório no Município de São Paulo.

La contaminación relacionada con el tráfico es un gran problema en los centros urbanos, y una gran parte de la población es vulnerable a sus efectos para la salud. El objetivo de este trabajo fue identificar la potencial asociación entre los internamientos hospitalarios por cáncer del aparato respiratorio con la densidad del tráfico vehicular en el Municipio de São Paulo, Brasil. Es un estudio ecológico con datos de internamientos hospitalarios por cáncer de los sistemas público (Autorización de Internación Hospitalaria - AIH) y particular (Comunicación de Internación Hospitalaria - CIH), de 2004 a 2006, geocodificados por dirección de residencia del individuo. Mediante el modelo ecológico de Besag-York-Mollié se evaluó inicialmente la relación entre el número de casos de internamiento por cáncer del aparato respiratorio en cada área de ponderación y covariables estandarizadas: densidad de tráfico e Índice de Desarrollo Humano Municipal (IDHM), como indicador de estatus socioeconómico. Secuencialmente, con un modelo clásico de Poisson, se procedió a una evaluación del riesgo asociado a las categorías crecientes de densidad de tráfico. El modelo de Besag-York-Mollié estimó un RR = 1,09 (IC95%: 1,02-1,15) y RR = 1,19 (IC95%: 1,10-1,29) de internamiento por cáncer del aparato respiratorio, para cada aumento de un desvío estándar de la densidad de tráfico e IDHM, respectivamente. Se evidenció también, a través del modelo de Poisson, un claro gradiente de exposición-respuesta para el internamiento por cáncer respiratorio (IRR = 1,11; IC95%: 1,07-1,15, para cada 10 unidades de incremento de la densidad de tráfico). Este trabajo sugiere que existe una asociación entre residir en áreas con alta densidad de tráfico y el internamiento por cáncer del aparato respiratorio en el Municipio de São Paulo.

Influência da densidade de tráfego veicular na internação por câncer do aparelho respiratório no Município de São Paulo, Brasil / Influence of vehicular traffic density on hospital admissions due to respiratory tract cancer in the city of São Paulo, Brazil / Influencia de la densidad de tráfico vehicular en el internamiento por cáncer del aparato respiratorio en el Municipio de São Paulo, Brasil

A poluição relacionada ao tráfego é um grande problema nos centros urbanos, e uma grande parcela da população fica vulnerável aos seus efeitos à saúde. Este trabalho teve como objetivo identificar potencial associação entre as internações hospitalares por câncer do aparelho respiratório com a densidade de tráfego veicular no Município de São Paulo, Brasil. É um estudo ecológico com dados de internações hospitalares por câncer dos sistemas público (Autorização de Internação Hospitalar - AIH) e particular (Comunicação de Internação Hospitalar - CIH), de 2004 a 2006, geocodificados por endereço de residência do indivíduo. Mediante um modelo ecológico de Besag-York-Mollié foi avaliada inicialmente a relação entre o número de casos de internação por câncer do aparelho respiratório em cada área de ponderação e as covariáveis padronizadas: densidade de tráfego e Índice de Desenvolvimento Humano Municipal (IDHM) como indicador de status socioeconômico. Sequencialmente, com um modelo clássico de Poisson, procedeu-se uma avaliação do risco associado às categorias crescentes de densidade de tráfego. O modelo de Besag-York-Mollié estimou um RR = 1,09 (IC95%: 1,02-1,15) e RR = 1,19 (IC95%: 1,10-1,29) de internação por câncer do aparelho respiratório, para cada aumento de um desvio padrão da densidade de tráfego e IDHM, respectivamente. Foi também evidenciado pelo modelo de Poisson um claro gradiente de exposição-resposta para internação por câncer respiratório (IRR = 1,11; IC95%: 1,07-1,15, para cada dez unidades de acréscimo da densidade de tráfego). Este trabalho sugere que há associação entre residir em áreas com alta densidade de tráfego e internação por câncer do aparelho respiratório no Município de São Paulo.

Pollution related to traffic is a major problem in urban centers and a large portion of the population is vulnerable to its health effects. This study sought to identify a potential association between hospital admissions due to respiratory tract cancer and vehicular traffic density in the city of São Paulo, Brazil. It is an ecological study of the public (Hospital Inpatient Authorization - AIH, in Portuguese) and private (Hospital Inpatient Communication - CIH, in Portuguese) health care systems, from 2004 to 2006, geocoded by individuals' residential addresses. Using a Besag-York-Mollié ecological model, we initially evaluated the relationship between number of cases of hospital admission due to respiratory tract cancer in each weighting area and the standardized co-variables: traffic density and Municipal Human Development Index (MHDI) as indicator of socioeconomic status. Using a classic Poisson model, we then evaluated the risk associated with growing traffic density categories. The Besag-York-Mollié model estimated a RR = 1.09 (95%CI: 1.02-1.15) and RR = 1.19 (95%CI: 1.10-1.29) of admission due to respiratory tract cancer for each increase of one standard deviation of traffic and MHDI, respectively. The Poisson model also showed a clear exposure-response gradient for admission due to respiratory tract cancer (IRR = 1.11; 95%CI: 1.07-1.15, for each 10 units of added traffic density). This study suggests that there is an association between residing in areas with high traffic density and hospital admissions due to respiratory tract cancer in the city of São Paulo.

La contaminación relacionada con el tráfico es un gran problema en los centros urbanos, y una gran parte de la población es vulnerable a sus efectos para la salud. El objetivo de este trabajo fue identificar la potencial asociación entre los internamientos hospitalarios por cáncer del aparato respiratorio con la densidad del tráfico vehicular en el Municipio de São Paulo, Brasil. Es un estudio ecológico con datos de internamientos hospitalarios por cáncer de los sistemas público (Autorización de Internación Hospitalaria - AIH) y particular (Comunicación de Internación Hospitalaria - CIH), de 2004 a 2006, geocodificados por dirección de residencia del individuo. Mediante el modelo ecológico de Besag-York-Mollié se evaluó inicialmente la relación entre el número de casos de internamiento por cáncer del aparato respiratorio en cada área de ponderación y covariables estandarizadas: densidad de tráfico e Índice de Desarrollo Humano Municipal (IDHM), como indicador de estatus socioeconómico. Secuencialmente, con un modelo clásico de Poisson, se procedió a una evaluación del riesgo asociado a las categorías crecientes de densidad de tráfico. El modelo de Besag-York-Mollié estimó un RR = 1,09 (IC95%: 1,02-1,15) y RR = 1,19 (IC95%: 1,10-1,29) de internamiento por cáncer del aparato respiratorio, para cada aumento de un desvío estándar de la densidad de tráfico e IDHM, respectivamente. Se evidenció también, a través del modelo de Poisson, un claro gradiente de exposición-respuesta para el internamiento por cáncer respiratorio (IRR = 1,11; IC95%: 1,07-1,15, para cada 10 unidades de incremento de la densidad de tráfico). Este trabajo sugiere que existe una asociación entre residir en áreas con alta densidad de tráfico y el internamiento por cáncer del aparato respiratorio en el Municipio de São Paulo.

Health Risks Associated with Occupational Exposure to Ambient Air Pollution in Commercial Drivers: A Systematic Review.

Ambient air pollution is a major global health problem and commercial drivers are particularly exposed to it. As no systematic assessment of the health risks associated with occupational exposure to ambient air pollution in this population had yet been carried out, we conducted a systematic review using a protocol-driven strategy. Papers published from inception to April 20, 2018 in MEDLINE, EMBASE, CINAHL, African journals online, the Cochrane library, ISRCTN WHO ICTRP, and the Web of Science and Scopus databases were screened for inclusion by two independent reviewers. Original articles with at least an available abstract in English or French were included. The initial search retrieved 1454 published articles of which 20 articles were included. Three studies reported a significant difference in white blood cells (106/L) among commercial motorcyclists compared to rural inhabitants (5.041 ± 1.209 vs. 5.900 ± 1.213, p = 0.001), an increased risk of lung cancer (RR = 1.6, 95%CI 1.5⁻1.8) in bus drivers and an increased standardized mortality ratio (SMR) in bus drivers from Hodgkin's lymphoma (SMR 2.17, 95%CI 1.19⁻3.87) compared to white-collar workers. Other studies also found that drivers had more oxidative DNA damage and chromosome breaks. Four papers failed to demonstrate that the drivers were more exposed to air pollution than the controls. Three other studies also reported no significant difference in lung function parameters and respiratory symptoms. The genetic polymorphisms of detoxifying enzymes were also not homogeneously distributed compared to the controls. There is some evidence that occupational exposure to ambient air pollution among commercial drivers is associated with adverse health outcomes, but the existing literature is limited, with few studies on small sample size, methodological weaknesses, and contradictory findings-thus, further research is recommended.

Effects of Leisure-Time and Transport-Related Physical Activities on the Risk of Incident and Recurrent Myocardial Infarction and Interaction With Traffic-Related Air Pollution: A Cohort Study.

BACKGROUND: Physical activity enhances the uptake of air pollutants, possibly reducing its beneficial effects. We examined the effects of leisure-time and transport-related physical activities on the risk of myocardial infarction (MI), and whether potential benefits on MI are reduced by exposure to traffic-related air pollution. METHODS AND RESULTS: A group of 57 053 participants (50-65 years of age) from the Danish Diet, Cancer, and Health cohort reported physical activity at baseline (1993-1997) and were linked to registry data on hospital contacts and out-of-hospital deaths caused by MI, until December 2015. Nitrogen dioxide levels were estimated at participants' baseline residences. We used Cox regressions to associate participation in sports, cycling, walking, and gardening with incident and recurrent MI, and tested for interaction by nitrogen dioxide. Of 50 635 participants without MI at baseline, 2936 developed incident MI, and of 1233 participants with MI before baseline, 324 had recurring MI during follow-up. Mean nitrogen dioxide concentration was 18.7 µg/m3 at baseline (1993-1997). We found inverse statistically significant associations between participation in sports (hazard ratio; 95% confidence interval: 0.85; 0.79-0.92), cycling (0.91; 0.84-0.98), gardening (0.87; 0.80-0.95), and incident MI, while the association with walking was statistically nonsignificant (0.95; 0.83-1.08). Recurrent MI was statistically nonsignificantly inversely associated with cycling (0.80; 0.63-1.02), walking (0.82, 0.57-1.16), and gardening (0.91; 0.71-1.18), and positively with sports (1.06; 0.83-1.35). There was no effect modification of the associations between physical activity and MI by nitrogen dioxide. CONCLUSIONS: Benefits of physical activity on both the incidence and the recurrence of MI are not reduced by exposure to high levels of air pollution.