Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent.
We examined the association between long-term exposure to ambient air pollution and ...incidence of postmenopausal breast cancer in European women.
In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM
, PM
, and PM
, respectively); PM
absorbance; nitrogen oxides (NO
and NO
); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.
Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM
{hazard ratio (HR)=1.08 95% confidence interval (CI): 0.77, 1.51 per 5 μg/m
}, PM
1.07 (95% CI: 0.89, 1.30) per 10 μg/m
, PM
1.20 (95% CI: 0.96, 1.49 per 5 μg/m
, and NO
1.02 (95% CI: 0.98, 1.07 per 10 μg/m
, and a statistically significant association with NO
1.04 (95% CI: 1.00, 1.08) per 20 μg/m
,
=0.04.
We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. https://doi.org/10.1289/EHP1742.
Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are used in a variety of consumer products and have been detected worldwide in human blood. Recent studies mainly of highly exposed ...populations have indicated that PFOA and PFOS may affect serum cholesterol levels, but the magnitude of the effect may be inconsistent across exposure levels. The aim of the present cross-sectional study was to investigate the association between plasma PFOA and PFOS and total cholesterol in a general, middle-aged Danish population. The study population comprised 753 individuals (663 men and 90 women), 50-65 years of age, nested within a Danish cohort of 57,053 participants. Blood samples were taken from all cohort members at enrolment (1993-1997) and stored in a biobank at -150°C. Plasma levels of PFOA and PFOS and serum levels of total cholesterol were measured. The associations between plasma PFOA and PFOS levels and total cholesterol levels were analysed by generalized linear models, both crude and adjusted for potential confounders. We observed statistically significant positive associations between both perfluorinated compounds and total cholesterol, e.g. a 4.4 95% CI = 1.1-7.8 higher concentration of total cholesterol (mg/dL) per interquartile range of PFOA plasma level. Sex and prevalent diabetes appeared to modify the association between PFOA and PFOS, respectively, and cholesterol. In conclusion, this study indicated positive associations between plasma PFOA and PFOS levels and total cholesterol in a middle-aged Danish population, although whether the observed pattern of results reflects a causal association is unclear.
Tobacco smoke exposure increases the risk of cancer in the liver, but little is known about the possible risk associated with exposure to ambient air pollution.
We evaluated the association between ...residential exposure to air pollution and primary liver cancer incidence.
We obtained data from four cohorts with enrolment during 1985–2005 in Denmark, Austria and Italy. Exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter of less than 10µm (PM10), less than 2.5µm (PM2.5), between 2.5 and 10µm (PM2.5–10) and PM2.5 absorbance (soot) at baseline home addresses were estimated using land-use regression models from the ESCAPE project. We also investigated traffic density on the nearest road. We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and random-effects meta-analyses to estimate summary hazard ratios (HRs) and 95% confidence intervals (CIs).
Out of 174,770 included participants, 279 liver cancer cases were diagnosed during a mean follow-up of 17 years. In each cohort, HRs above one were observed for all exposures with exception of PM2.5 absorbance and traffic density. In the meta-analysis, all exposures were associated with elevated HRs, but none of the associations reached statistical significance. The summary HR associated with a 10-μg/m3 increase in NO2 was 1.10 (95% confidence interval (CI): 0.93, 1.30) and 1.34 (95% CI: 0.76, 2.35) for a 5-μg/m3 increase in PM2.5.
The results provide suggestive evidence that ambient air pollution may increase the risk of liver cancer. Confidence intervals for associations with NO2 and NOX were narrower than for the other exposures.
•Tobacco smoke increases liver cancer risk but risk of air pollution is less studied.•Residential exposure to ambient air pollution for 4 European cohorts was assessed.•Exposure to ambient air pollution at residence may increase the risk of liver cancer.
Background & Aims Antioxidant intake has been reported to increase the risk of colorectal cancer (CRC) for smokers, yet reduce the risk for nonsmokers. We investigated the association between tobacco ...smoking and risk of colon or rectal cancer, and whether dietary and supplemental intake of the antioxidant vitamins A, C, E, β-carotene, selenium, zinc, and manganese affects the risk of CRC among smokers. Methods Data on smoking habits and antioxidant intake were analyzed for 54,208 participants in the Danish Prospective Diet, Cancer and Health Study. Of these participants, 642 were diagnosed with colon cancer and 348 were diagnosed with rectal cancer. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazard models. Principal components were used to analyze intake of combinations of antioxidants. Results Ever smoking increased the risk for CRC (hazard ratio, 1.19; 95% confidence interval, 1.03–1.37), especially for rectal cancer. Smoking for at least 20 years was associated with a 26% increase in risk of CRC, compared with never smokers, and smoking 20 g tobacco or more each day was associated with a 30% increase in risk. Smoking for more than 30 years, or more than 20 g tobacco each day, was associated with a 48% increase in risk of rectal cancer. We did not observe an interaction between smoking and antioxidant consumption on risk of CRC. Conclusions Tobacco smoking increases the risk for CRC. We did not observe that consumption of antioxidant micronutrients modulates the effects of smoking on CRC risk.
Non-Hodgkin lymphoma (NHL) is the most common hematologic malignancy in the world. Involvement of organochlorines has been proposed in disease etiology. No study has investigated organochlorine ...exposure in relation to survival after a NHL diagnosis.
In a survivor cohort consisting of 232 NHL cases from the Danish Diet, Cancer and Health cohort, we examined the association between adipose tissue organochlorine concentrations polychlorinated biphenyls (PCBs) and pesticides and subsequent survival, using Cox proportional hazards models.
We found no statistically significant association between organochlorine concentrations and subsequent survival. If anything, there was a nonsignificant tendency toward an inverse association with PCBs, but not pesticides.
In conclusion, the current study does not support an increased risk of death among NHL patients with high tissue concentrations of organochlorines.
This is the first study to investigate adipose organochlorine concentrations and survival after a NHL diagnosis.
.
...changes in bronchial responsiveness and asthma symptoms have been demonstrated in relation to the menstrual cycle.1 These findings suggest that treatment with exogenous sex hormones, such as ...postmenopausal hormone replacement therapy (HRT), may affect the risk for asthma morbidity, and this is supported by several observational studies showing increased asthma prevalence and incidence in women using HRT.2-6 Still, HRT is not considered an established risk factor for asthma in clinical guidelines.7 Hospital admission for asthma, due to acute exacerbations or difficult to control disease, represents severe disease with major impact on quality of life of the individual and health care expenditures. Furthermore, a causal role of HRT in the pathogenesis of asthma exacerbations is biologically plausible and in keeping with considerable epidemiological and experimental evidence of a role of sex hormones in asthma pathology.1 Our results are in agreement with several previous studies on milder asthma observed in both cross-sectional3-5 and longitudinal studies.2,6 We also observed an association between HRT and hospital admission for COPD but with smaller effect estimates than seen for asthma.\n0) Time since HRT cessation (y), mean ± SD -- -- 2.7 ± 4.6 Table E1 Characteristics of 22,958 women in the Diet, Cancer and Health cohort total and by HRT use status Values are n (%) unless indicated otherwise.BMI, Body mass index.
Background: Previous studies have shown associations between air pollution and risk for lung cancer. Objective: We investigated whether traffic and the concentration of nitrogen oxides (NOx) at the ...residence are associated with risk for lung cancer. Methods: We identified 592 lung cancer cases in the Danish Cancer Registry among 52,970 members of the Diet, Cancer and Health cohort and traced residential addresses from 1 January 1971 in the Central Population Registry. We calculated the NOx concentration at each address by dispersion models and calculated the time-weighted average concentration for all addresses for each person. We used Cox models to estimate incidence rate ratios (IRRs) after adjustment for smoking (status, duration, and intensity), environmental tobacco smoke, length of school attendance, occupation, and dietary intake of fruit. Results: For the highest compared with the lowest quartile of NOx concentration at the residence, we found an IRR for lung cancer of 1.30 95% confidence interval (CI), 1.05-1.61, and the IRR for lung cancer in association with living within 50 m of a major road (> 10,000 vehicles/day) was 1.21 (95% CI, 0.95–1.55). The results showed tendencies of stronger associations among nonsmokers, among those with a relatively low fruit intake, and among those with a longer school attendance; only length of school attendance modified the effect significantly. Conclusions: This study supports that risk for lung cancer is associated with different markers of air pollution from traffic near the residence.
Both road traffic noise and ambient air pollution have been associated with risk for ischemic heart disease, but only few inconsistent studies include both exposures.
In a population-based cohort of ...57 053 people aged 50 to 64 years at enrolment in 1993-1997, we identified 1600 cases of first-ever MI between enrolment and 2006. The mean follow-up time was 9.8 years. Exposure to road traffic noise and air pollution from 1988 to 2006 was estimated for all cohort members from residential address history. Associations between exposure to road traffic noise and incident MI were analysed in a Cox regression model with adjustment for air pollution (NO(x)) and other potential confounders: age, sex, education, lifestyle confounders, railway and airport noise.
We found that residential exposure to road traffic noise (L(den)) was significantly associated with MI, with an incidence rate ratio IRR of 1.12 per 10 dB for both of the two exposure windows: yearly exposure at the time of diagnosis (95% confidence interval (CI): 1.02-1.22) and 5-years time-weighted mean (95% CI: 1.02-1.23) preceding the diagnosis. Visualizing of the results using restricted cubic splines showed a linear dose-response relationship.
Exposure to long-term residential road traffic noise was associated with a higher risk for MI, in a dose-dependent manner.
Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A ...Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM
), nitrogen dioxide (NO
) and black carbon (BC) with asthma incidence in adults.
We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders.
Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 μg·m
for PM
, 1.17 (95% CI 1.10-1.25) per 10 µg·m
for NO
and 1.15 (95% CI 1.08-1.23) per 0.5×10
m
for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM
and NO
. NO
and BC estimates remained unchanged in two-pollutant models with PM
, whereas PM
estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold.
Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.
Synthetically produced perfluorinated chemicals (PFCs) are widely used in industrial products because of their anti-wetting and surfactant properties. PFCs are suspected carcinogens and a possible ...mechanism of action is generation of oxidative stress. We have investigated the potential of five different PFCs to generate reactive oxygen species (ROS) and to induce oxidative DNA damage in HepG2 cells. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) increased the intracellular ROS production by 1.52-fold (95% CI, 1.37–1.67) and 1.25-fold (95% CI, 1.10–1.40), respectively. However, the increase in ROS production was not concentration-dependent and the compounds did not generate DNA damage that could be detected by the alkaline comet assay as strand breakage and alkali-labile sites or formamidopyrimidine-DNA-glycosylase (FPG) sites. Perfluorobutane sulfonate (PFBS) and perfluorohexanoic acid (PFHxA) did not generate ROS or DNA damage. Only the exposure to perfluorononanoic acid (PFNA) caused a modest increase in DNA damage at a cytotoxic concentration level, which was detected as lactate dehydrogenase (LDH) release into the cell medium. This was not related to ROS generation. Collectively, these results indicate that PFCs induce only modest effects in terms of ROS production and DNA damage in a cell line representing the human liver.
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