Abstract

8532 Background: Health effects associated with particles less than 2.5 μm in diameter (PM2.5) have been well studied, leading to the establishment of air quality standards and routine monitoring. Additionally, there is growing experimental evidence that ultrafine particles (UFPs), defined as particles less than 0.1µm in diameter, may adversely affect lung health, eliciting greater injury than larger particles due to deeper penetration into airways and longer retention in the lung parenchyma. Only two epidemiological studies have investigated this topic, finding no associations between ambient UFPs and respiratory mortality or overall lung cancer incidence respectively. Given the limited epidemiologic investigation of UFPs and lung cancer, we examined the association between airport-related UFPs and lung cancer incidence in a large, racially and ethnically diverse cohort. Methods: We estimated airport-related UFP exposure for 71,387 participants of the Multiethnic Cohort, who lived within a 53 km×43 km grid area around the Los Angeles International Airport (LAX) from date of cohort entry (1993-1996) through December 31, 2013. Cox proportional hazards regression was used, with calendar month/year as the time variable, to examine associations between UFP exposure and lung cancer risk adjusting for demographics, lifetime smoking, neighborhood socioeconomic status, occupation and lifestyle factors. Subgroup analyses were conducted by racial and ethnic groups, lung cancer histology, and smoking status. Co-pollutant models were run to mutually adjust for other traffic-related air pollutants. Results: A per unit increase in the interquartile range (IQR) of airport-related UFP exposure was not associated with lung cancer risk overall [HR = 1.01, 95% CI: 0.97-1.05] or by race and ethnicity. UFP exposure was suggestive of a positive association with risk of lung squamous cell carcinoma (SCC) [HR per IQR = 1.08, 95% CI: 1.00-1.17]. No associations were observed for other histologies [Phet for histology = .05]. UFP exposure was associated with an increased SCC risk among current smokers [HR = 1.11, 95% CI: 1.01-1.22] but not among never or past smokers [Phet for smoking = 0.51]. Conclusions: This study suggests a possible association between airport-related UFP exposure and risk of SCC. These results may be explained by previous studies finding that UFPs activate genes involved in oxidative damage, TNF-α signaling via NF-κB, and secretion of inflammatory and cardiopulmonary disease biomarkers. These findings warrant further investigation in large epidemiologic cohorts.

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