METHODS: This cross-sectional nationwide study conducted in 2018 recruited convenience sample of 289 parents with children up to age 12 at public areas. Parents were asked to rate the risk level from 1 (no risk) to 5 (extremely high risk) by looking at photographs of an adult smoking in the presence of a child in 8 different situations. The implementation of smoking restriction rules was assessed. Mean scores were calculated with higher scores representing higher risk perception of SHS to child's health. Linear regression analysis was used to determine factors associated with the level of parental risk perception of SHS exposure to their children's health.
RESULTS: A total of 246 parents responded. Their mean age was 35 years (SD 6.4). The majority were mothers (75.6%), Malays (72.0%) and had tertiary education level (82.5%), and non-smoker (87.1%). The mean age of respondents' youngest child was 3 years (SD 3.1). The risk perception level was high [mean scores: 4.11 (SD: 0.82)]. Most parents implemented household (65.0%) and car (68.3%) smoking restriction rules. Lower levels of risk perception were observed among participants who were current smokers (p
Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.
Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.
Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.
OBJECTIVE: To evaluate the association between long-term exposure to ambient air pollution and BC incidence.
DESIGN, SETTING, AND PARTICIPANTS: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NOx), particulate matter (PM) with diameter <10μm (PM10), <2.5μm (PM2.5), between 2.5 and 10μm (PM2.5-10), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project.
OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence.
RESULTS AND LIMITATIONS: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval [CI] 0.89-1.08) and 0.86 (95% CI 0.63-1.18), respectively. Limitations include the lack of information about lifetime exposure.
CONCLUSIONS: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC.
PATIENT SUMMARY: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at place of residence and bladder cancer risk.
METHODS: This was a prospective, cross sectional study recruiting injured motorcyclists from Hanoi, Vietnam hospital. The participants were interviewed by a trained researcher. The participants' helmets were collected post-crash. Initially, the helmets were examined for their type and external characteristics. A 3 cm × 3 cm cut was made on the helmet in the impacted and non-impacted areas (control). These areas were investigated for evidence of POD and presence of micro-cracks and material disintegration. 50 participants were enrolled. Sources of information included questionnaire and laboratory analyses. The helmet factors of interest were age of the helmet, exposure of helmet to sunlight and rain (duration/day) and history of previous impact. Laboratory analyses included Fourier Transform Infra Red (FTIR) for degradation and scanning electron microscopy (SEM) for micro-structural examination.
RESULTS: Majority of the helmets was the open-face type, 40 (80.0%). 31 (62.0%) helmets aged less than three years (LTY) and 19 (38.0%) were three years old or more (MTY). 19 (61.3%) of the LTY helmets and 12 (63.2%) MTY helmets showed evidence of POD. The duration of helmet exposure to sunlight was between 93 to 6570 hours (mean 2347.74 hours; SD 1733.39). The SEM showed 15 helmets (30%) with micro-fractures, 21 helmets (42.0%) with material disintegration. Prolonged uv exposure to the ABS helmets resulted in changes in the helmet material in the form of material disintegration and microcracks and this association was statistically significant (p = 0.03).
CONCLUSION: POD occurs due to routine exposure to the ultraviolet light. Prolonged uv exposure affects outer shell surface material integrity.