Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Chimerica: the acrid scent of success

Air pollution: another cause of lung cancer

Background: Ambient air pollution, and in particular particulate matter (PM), is suspected to cause lung cancer. Aims: To estimate associations between long-term exposure to air pollution at the residence and lung cancer incidence in European populations. Methods: We used individual data from 17 European cohorts. Baseline addresses were geocoded and air pollution was assessed by land-use regression models for PM below 10 µm (PM10), below 2.5 µm (PM2.5), between 2.5 and 10 µm (PMcoarse), PM2.5absorbance, nitrogen oxides and two traffic indicators. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses of the cohort-specific results. Results: We included 312,944 cohort members contributing 4,013,131 person-years at risk and 2095 incident lung cancer cases developed during the follow-up of on average 12.8 years. The meta-analyses showed that a 10 µg/m3 increase in PM10 was associated with a 22% (95% confidence interval [CI]: 3 to 45%) increase in risk for lung cancer, a 5 µg/m3 increase in PM2.5 was associated with an 18% (95% CI: -4 to 46%) increase in risk. Similar increments of PM10 and PM2.5, respectively, were associated with 49% (95% CI: 8 to 105%) and 55% (95% CI: 5 to 129%) increase in risk for adenocarcinomas of the lung. An increase in road traffic of 4000 vehicle-km/day within 100 m of the residence was associated with a 9% (95% CI: -1 to 21%) increase in risk for lung cancer. Associations between PM air pollution and lung cancer were also detected among never smokers. The results showed no association for nitrogen oxides or traffic on nearest street. Conclusions: This study showed associations between particulate matter air pollution and lung cancer incidence in Europe.

Cleaning our polluted skies

Background and aimsFew studies on long-term exposure to air pollution and mortality and lung cancer incidence have been reported from Europe. Within the multi-center European Study of Cohorts for Air Pollution Effects (ESCAPE) we investigated the association between mortality and lung cancer incidence, and long-term exposure to multiple air pollutants. MethodsData from 16-22 European cohort studies were used. Residential exposure was assessed following a strictly standardized protocol as annual average concentrations of particles less than 2.5µm (PM2.5), less than 10µm (PM10), and between 10µm and 2.5µm (PMcoarse), PM2.5 absorbance, and nitrogen oxides (NO2 and NOx) using Land Use Regression (LUR) models. Cohort-specific statistical analyses using confounder models with increasing level of adjustment were conducted using Cox proportional hazards models using a common protocol. Random-effects meta-analysis was used to obtain pooled effect estimates.Results The total study population consisted of ~300,000 p...

Background:There is a positive association between ambient fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) and incidence and mortality of lung cancer (LC), but few studies have assessed the relationship between ambient PM2.5 and LC among never smokers.Objectives:We assessed the association between PM2.5 and risk of LC using the Adventist Health and Smog Study-2 (AHSMOG-2), a cohort of health conscious nonsmokers where 81% have never smoked.Methods:A total of 80,285 AHSMOG-2 participants were followed for an average of 7.5 years with respect to incident LC identified through linkage with U.S. state cancer registries. Estimates of ambient air pollution levels at participants’ residences were obtained for 2000 and 2001, the years immediately prior to the start of the study.Results:A total of 250 incident LC cases occurred during 598,927 person-years of follow-up. For each 10-μg/m3 increment in PM2.5, adjusted hazard ratio (HR) with 95% confidence interval (CI) for LC incidence was 1.43 (95% CI: 1.11, 1.84) in the two-pollutant multivariable model with ozone. Among those who spent > 1 hr/day outdoors or who had lived 5 or more years at their enrollment address, the HR was 1.68 (95% CI: 1.28, 2.22) and 1.54 (95% CI: 1.17, 2.04), respectively.Conclusion:Increased risk estimates of LC were observed for each 10-μg/m3 increment in ambient PM2.5 concentration. The estimate was higher among those with longer residence at enrollment address and those who spent > 1 hr/day outdoors.Citation:Gharibvand L, Shavlik D, Ghamsary M, Beeson WL, Soret S, Knutsen R, Knutsen SF. 2017. The association between ambient fine particulate air pollution and lung cancer incidence: results from the AHSMOG-2 study. Environ Health Perspect 125:378–384; http://dx.doi.org/10.1289/EHP124Citation: Gharibvand L, Shavlik D, Ghamsary M, Beeson WL, Soret S, Knutsen R, Knutsen SF. 2017. The association between ambient fine particulate air pollution and lung cancer incidence: results from the AHSMOG-2 study. Environ Health Perspect 125:378–384; http://dx.doi.org/10.1289/EHP124

Background:Ambient air pollution is classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, epidemiologic studies supporting this classification have focused on lung cancer mortality rather than incidence, and spatial and temporal resolutions of exposure estimates have varied considerably across studies.Methods:We evaluated the association of outdoor air pollution and lung cancer incidence among never-smoking participants of the Women’s Health Initiative (WHI) study, a large, US-based cohort of postmenopausal women (N = 65,419; 265 cases). We used geospatial models to estimate exposures to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) based on residential addresses at baseline and throughout follow-up. We also characterized exposures to traffic-related air pollution by proximity to major roadways. We estimated hazard ratios (HRs) for the risk of lung cancer in association with these exposure metrics using Cox proportional hazards regression models.Results:No compelling associations of PM2.5 and NO2 exposures with lung cancer risk were observed. An increased risk of lung cancer was observed when comparing those individuals with residences <50 versus ≥200 meters from a primary limited access highway (HR = 5.23; 95% confidence interval = 1.94, 14.13).Conclusions:Our results do not exclude lung cancer risk estimates observed in association with PM2.5 and NO2 exposures identified in previous studies. Our results suggest that residential proximity to major roadways may be a proxy for carcinogenic exposures not correlated with PM2.5 or NO2 levels. New studies of air pollution and lung cancer incidence should characterize additional aspects of proximity to major roadways.

In utero exposures to certain toxic constituents of traffic-related air pollution have been linked to neurological impairments. Recent studies have addressed whether exposures to such air toxicants might be environmental risk factors for autism spectrum disorders (ASDs)—developmental disabilities that can involve rigid, repetitive behaviors and impairments in communication and social interactions. Although several past studies reported associations between ASDs and certain air pollutants, a new analysis of four prospective cohorts published in this issue of EHP appears to contradict those findings, reporting no such associations.1 Working as part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) project,2 the researchers analyzed data from four different prospective cohorts investigating ASDs in relation to air pollution. These studies assessed autistic traits, but not formal diagnoses of an ASD, in more than 8,000 children in the general population. The presence of autistic traits had been assessed using validated screening tests, which varied in the included studies. The authors of the current study used land-use regression models to estimate mothers’ at-home exposures to nitrogen oxides (NOx) and various sizes of particulate matter (PM) during pregnancy.1 Although several earlier studies reported a higher prevalence of autism in children exposed prenatally to traffic-related air pollutants, a new analysis of four prospective cohorts finds no such association. Depending on the study, 0.7–3.6% of these children—mostly boys—showed autistic traits in the clinical range, and 3.2–12.3% showed traits in the clinical/borderline range. In the final analysis, no associations were found between presence of autistic traits and prenatal exposure to any of the air pollutants.1 “Almost all previous studies carried out mainly in the United States found an association between air pollution and ASDs,” says lead author Monica Guxens, an assistant research professor at the Centre for Research in Environmental Epidemiology in Barcelona. “I do not think that ASDs are different in Europe than in the U.S., but the best way to check what is going on here is to try to replicate the U.S. studies in Europe following a similar study design.” Bing-Fang Hwang, a professor of environmental and occupational epidemiology at China Medical University, points out that in three of the studies parents assessed their children’s traits, while psychologists assessed traits in the fourth. “I do not think it’s appropriate to combine all results through meta-analysis without considering the heterogeneity of different diagnoses from parents and a psychologist,” he says. “It may cause bias in estimation of combined odds ratio. The results should be interpreted cautiously.” The authors acknowledge this and other limitations in their paper. However, the consistent null findings across cohorts suggest their results are not spurious and must be investigated further.1 Raanan Raz, an epidemiologist at the Hebrew University of Jerusalem-Hadassah, says the study is important because it examines the issue of air pollution and autism in a new approach—looking at autistic traits in prospective cohorts of children enrolled at birth. He says, “The researchers interpreted [results] with appropriate caution, stating the possible explanations in their discussion.” Among those possible explanations, the authors hypothesize that cohorts of children like the ones in their study would have a vanishingly small proportion of the extreme autism phenotypes that appear in case–control studies.1

India launches air quality index to tackle pollution problems

BackgroundEpidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.MethodsIn 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.ResultsOf 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.ConclusionWe 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.

Background: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.Objectives: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.Methods: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis.Results: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated.Conclusions: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.Citation: Fuks KB, Weinmayr G, Foraster M, Dratva J, Hampel R, Houthuijs D, Oftedal B, Oudin A, Panasevich S, Penell J, Sommar JN, Sørensen M, Tittanen P, Wolf K, Xun WW, Aguilera I, Basagaña X, Beelen R, Bots ML, Brunekreef B, Bueno-de-Mesquita HB, Caracciolo B, Cirach M, de Faire U, de Nazelle A, Eeftens M, Elosua R, Erbel R, Forsberg B, Fratiglioni L, Gaspoz JM, Hilding A, Jula A, Korek M, Krämer U, Künzli N, Lanki T, Leander K, Magnusson PK, Marrugat J, Nieuwenhuijsen MJ, Östenson CG, Pedersen NL, Pershagen G, Phuleria HC, Probst-Hensch NM, Raaschou-Nielsen O, Schaffner E, Schikowski T, Schindler C, Schwarze PE, Søgaard AJ, Sugiri D, Swart WJ, Tsai MY, Turunen AW, Vineis P, Peters A, Hoffmann B. 2014. Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Environ Health Perspect 122:896–905; http://dx.doi.org/10.1289/ehp.1307725

Particulate matter air pollution components and risk for lung cancer

Outdoor air pollution and lung cancer: recent epidemiologic evidence.

Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project

Development of NO2 and NOx land use regression models for estimating air pollution exposure in 36 study areas in Europe – The ESCAPE project