Contributions of alkenes to cancer risk from urban air pollution were estimated on the basis of radiation dose equivalent of target dose. The latter was inferred from the incremental carboxyhaemoglobin (COHb) level in urban areas, the ratio of epoxide-haemoglobin adducts to COHb levels in smokers and the alkenes/CO level ratios in cigarette smoke and urban air. This model predicts some 200 and 5 cancer cases annually in Sweden from ethene and propene, respectively. This indicates that the risk from alkenes is of the same order of magnitude as that from the particulate fraction of the pollution.
In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 µm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6% (95% confidence interval: 1, 11) and 4% (95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22% (95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.
Inconsistent results have been obtained from studies that have examined the relationship between air pollution and hospital visits for stroke. We undertook a time-stratified case-crossover study to evaluate associations between outdoor air pollution and emergency department visits for stroke among the elderly according to stroke type, season, and sex. Analyses are based on a total of 12,422 stroke visits among those 65 years of age and older in Edmonton, Canada between April 1, 1992 and March 31, 2002. Daily air pollution levels for SO(2), NO(2), PM(2.5), PM(10), CO and O(3) were estimated using data from fixed-site monitoring stations. Particulate matter data were only available from 1998 onwards. Conditional logistic regression was used to estimate the odds ratios (ORs) and their 95% confidence intervals in relation to an increase in the interquartile range (IQR) of each pollutant. ORs were adjusted for the effects of temperature and relative humidity. We found no association between outdoor measures of air pollution and all stroke visits. In contrast, elevated risks were observed between levels of air pollution and acute ischemic stroke between April and September. During this season, the ORs associated with an increase in the IQR of the 3-day average for CO and NO(2) were 1.32 (95% CI = 1.09-1.60) and 1.26 (95% CI = 1.09-1.46), respectively. CO exposures in the same season, lagged 1 day, were associated with an increased risk of hemorrhagic stroke with ORs was 1.20 (95% CI = 1.00-1.43). Our results suggest it is possible that vehicular traffic, which produces increased levels of NO(2) and CO, contributes to an increased incidence of emergency department visits for stroke.
Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion.
To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality.
This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter
Recent reviews conclude an association between traffic-related pollution and incidence of asthma in children, but not all studies agree. Studies have almost exclusively relied on parental-reported symptoms or parental-reported diagnoses of asthma and wheeze. Our aim was to investigate if traffic exposure is associated with higher incidence of early onset asthma, using registry-based outcome data.
We investigated a birth cohort in southern Sweden, consisting of N = 26,128 children with outcome and exposure data (born July 2005-2010). Of these children, N = 7898 had additional covariate information. The cohort was followed to the end of 2011.Traffic intensity, and dispersion-modeled concentrations of NOX (100×100 m grid), at residential addresses, were linked with registry data on dispensed asthma medication (the Swedish Prescribed Drug Register), and hospital and primary health care diagnoses of bronchiolitis, obstructive bronchitis and asthma (The Scania Health Care Register).Covariate information was obtained from questionnaires distributed to parents at Child Health Care-centre visits, eight months after birth. Cox proportional hazards regression was used for the statistical analyses.
Living in close proximity to a road with =8640 cars/day (compared to 0-8640 cars/day), was not associated with higher incidence of first purchase of inhaled ß2-agonist (adjusted hazard ratio (adj.HR) = 0.9, 95% CI: 0.8-1.0); third year purchase of inhaled ß2-agonist (adj.HR = 0.7, 95% CI: 0.6-0.9); bronchiolitis (adj.HR = 0.7, 95% CI: 0.6-0.9), obstructive bronchitis (adj.HR = 1.0, 95% CI: 0.9-1.2), or asthma (adj.HR = 0.7, 95% CI: 0.6- 0.9). Similar results were found for inhaled corticosteroids, and in relation to NOX.
Traffic-related exposure was not associated with higher incidence of asthma medication, or diagnoses of asthma, bronchiolitis, or obstructive bronchitis, in children 0-6 years in southern Sweden. This may depend on the low levels of traffic pollution in the area, mainly well below the WHO-guideline for NO2.
Despite of the fact that engine manufacturers develop a new technology to reduce exhaust emissions, insufficient attention given to particulate emissions. However, diesel exhaust particles are a major source of air-borne pollution, contain vast amount of polycyclic aromatic hydrocarbons (PAHs) and may have deleterious effects on the immune system, resulting in the induction and enhancement of pro-allergic processes. In the current study, vehicle emitted particles (VEP) from 2 different types of cars (diesel - D and gasoline - G) and locomotive (L) were collected. Overall, 129 four-week-old, male SPF-class Kunming mice were subcutaneously instilled with either low dose 100, 250 or high dose, 500mg/kg VEP and 15 mice were assigned as control group. The systemic toxicity was evaluated and alterations in the percentages of the CD3, CD4, CD8, CD16, CD25 expressing cells, basophils, eosinophils and neutrophils were determined. Basophil percentages were inversely associated with the PAH content of the VEPs, however basophil sensitization was more important than cell count in VEP exposure. Thus, the effects of VEP-PAHs emerge with the activation of basophils in an allergen independent fashion. Despite the increased percentage of CD4+ T cells, a sharp decrease in basophil counts at 500mg/kg of VEP indicates a decreased inhibitory effect of CD16+ monocytes on the proliferation of CD4+ T cell and suppressed polarization into a Th2 phenotype. Therefore, although the restrictions for vehicles emissions differ between countries, follow up studies and strict regulations are needed.
The objective of this article was to find associations between cancer of the mouth and pharynx, occupation and chemical exposure. A cohort of Finns born between 1906 and 1945 was followed-up for 46.8 (21.5 in males and 25.3 in females) million person-years during 1971-95. Incident cases of cancer of the mouth and pharynx (n = 2,708) were identified in a record linkage with the Finnish Cancer Registry. The Census occupations in 1970 were converted to chemical exposures with a job-exposure matrix (FINJEM). Cumulative exposure (CE) was calculated as the product of prevalence, level and duration of the exposure. Standardized incidence ratio (SIR) was calculated for each of the 393 occupations, and for CE categories of the 43 chemical agents, using total Finnish population as reference. Relative risks (RR) comparing various CE-categories with unexposed ones were defined for selected agents by Poisson regression analysis. Elevated SIRs were observed among lawyers, authors, journalists, performing artists, musicians, electronics and telefitters, painters (building), building hands, dockers, unskilled labourers and hotel porters in males and private secretaries, dressmakers, shoemakers and cobblers, waiters, pursers and stewardesses in females. The multivariate analyses showed high RRs for high exposure to aliphatic and alicyclic hydrocarbons, pesticides and alcohol. In conclusion, occupations with high SIRs were mostly the ones with high consumption of alcohol. Exposure to solvents and possibly to pesticides, engine exhaust, textile dust and leather dust may increase the risk of cancer of mouth and pharynx.
Exposure to road traffic noise and air pollution have both been associated with risk for stroke. The few studies including both exposures show inconsistent results. We aimed to investigate potential mutual confounding and combined effects between road traffic noise and air pollution in association with risk for stroke. In a population-based cohort of 57,053 people aged 50-64 years at enrollment, we identified 1999 incident stroke cases in national registries, followed by validation through medical records. Mean follow-up time was 11.2 years. Present and historical residential addresses from 1987 to 2009 were identified in national registers and road traffic noise and air pollution were modeled for all addresses. Analyses were done using Cox regression. A higher mean annual exposure at time of diagnosis of 10 µg/m(3) nitrogen dioxide (NO2) and 10 dB road traffic noise at the residential address was associated with ischemic stroke with incidence rate ratios (IRR) of 1.11 (95% CI: 1.03, 1.20) and 1.16 (95% CI: 1.07, 1.24), respectively, in single exposure models. In two-exposure models road traffic noise (IRR: 1.15) and not NO2 (IRR: 1.02) was associated with ischemic stroke. The strongest association was found for combination of high noise and high NO2 (IRR=1.28; 95% CI=1.09-1.52). Fatal stroke was positively associated with air pollution and not with traffic noise. In conclusion, in mutually adjusted models road traffic noise and not air pollution was associated ischemic stroke, while only air pollution affected risk for fatal strokes. There were indications of combined effects.
Dioxins and airborne fine particles are both environmental health problems that have been the subject of active public debate. Knowledge on fine particles has increased substantially during the last 10 years, and even the current, lowered levels in the Europe and in the United States appear to be a major public health problem. On the other hand, dioxins are ubiquitous persistent contaminants, some being carcinogens at high doses, and therefore of great concern. Our aim was to (a) quantitatively analyze the two pollutant health risks and (b) study the changes in risk in view of the current and forthcoming EU legislations on pollutants. We performed a comparative risk assessment for both pollutants in the Helsinki metropolitan area (Finland) and estimated the health effects with several scenarios. For primary fine particles: a comparison between the present emission situation for heavy-duty vehicles and the new fine particle emission standards set by the EU. For dioxins: an EU directive that regulates commercial fishing of Baltic salmon and herring that exceed the dioxin concentration limit set for fish meat, and a derogation (= exemption) from the directive for these two species. Both of these two decisions are very topical issues and this study estimates the expected changes in health effects due to these regulations. It was found that the estimated fine particle risk clearly outweighed the estimated dioxin risk. A substantial improvement to public health could be achieved by initiating reductions in emission standards; about 30 avoided premature deaths annually in the study area. In addition, the benefits of fish consumption due to omega-3 exposure were notably higher than the potential dioxin cancer risk. Both regulations were instigated as ways of promoting public health.